Ammonia nitrogen is a common contaminant in aquatic environments, and its potential toxicity to organisms has attracted extensive attention. However, few studies have comprehensively evaluated the negative impacts of ammonia stress on cold-water fish. In this study, liver, gill, and intestine specimens of Amur grayling (Thymallus grubii) from three treatment groups (control (0 mg/L), low ammonia (43.683 mg/L), and high ammonia (436.8 mg/L)), were collected for histological observation, biochemical examination, and transcriptomic, metabolomic, and intestinal microbiome analysis. Our results showed that excessive ammonia nitrogen blocked the normal immune function and compromised the integrity of liver and gill tissues through oxidative stress-mediated differential cell death pathways. Meanwhile, the multi-omics analysis revealed that ammonia exposure predominantly altered the carbohydrate, lipid, and amino acid metabolism modes. In addition, it was also demonstrated that ammonia nitrogen stress affected the composition of intestinal microbiota taxa. This study provides insights into the potential risks and hazards of ammonia stress on cold fish in natural waters and provides a reference for the environment control of the water quality in aquaculture.

The development of effective and safe dietary supplements is essential for both the prevention and management of ulcerative colitis (UC), as its pathogenesis is intricate and difficult to completely resolve. Crataegus pinnatifida, a medicinal food with a long history of use, has broad medicinal value. Recent research has revealed promising insights into the role of polysaccharide derived from Crataegus pinnatifida on modulating short-chain fatty acids (SCFAs) to alleviate UC inflammation. However, the mechanisms by which CPP regulates the intestinal microbiota and key metabolites during the antagonistic phase of UC have yet to be elucidated.

This research elucidated the protective role of CPP in relation to UC, highlighted the mechanisms through which CPP operates, particularly regarding gut microbiota and metabolism, and offered a theoretical foundation for the potential use of CPP as a dietary supplement aimed at preventing UC.

The impact of CPP on acute UC induced by 3 % DSS in mice was examined through the evaluation of the disease activity index, measurement of colon length, and observation of body weight changes. Enzyme-linked immunosorbent assay (ELISA) was used to measure inflammatory factor levels in both serum and colon, as well as to assess oxidative stress mediators. The intestinal histological damage, mucus layer damage and the level of tight junction protein were analyzed by histopathological staining and western blot (WB). The impact of gut microbiota on CPP in colitis was evaluated using 16S rRNA sequencing, microbiota depletion experiments, and fecal microbiota transplantation (FMT) studies. The key metabolic pathways and key metabolites affected by CPP in the treatment of UC were analyzed through untargeted metabolomics sequencing, ELISA, and WB assays.

Prophylactic dietary supplementation with Crataegus pinnatifida polysaccharide (CPP) notably reduced the fundamental clinical manifestations of UC induced by DSS, including DAI score, reduced colon length, and weight loss, as well as inflammation and oxidative stress. CPP promoted the expression of Claudin-1, ZO-1 and Occludin and promoted mucin secretion, which contributed to the mitigation of intestinal barrier damage caused by DSS. 16S sequencing results and metabolomics results revealed that CPP intervention upregulated the relative abundance of Lactobacillus, thereby reshaping the intestinal microbiota and activate the arginine biosynthesis pathway. The results of fecal microbiota transplantation and antibiotic clearance experiments indicated that the alleviating effect of CPP on UC was dependent on the intestinal microbiota and this alleviating effect was transferred through fecal microbiota transplantation. Mechanistically, CPP indirectly promoted the expression of the rate-limiting enzyme argininosuccinate synthase 1 (ASS1) in the intestinal Arginine biosynthesis pathway by reshaping the intestinal microbiota, thereby increasing intestinal Arginine level and alleviating the inflammatory response and oxidative stress induced by DSS and intestinal barrier damage.

Our research findings demonstrate that CPP is a plant-derived polysaccharide that alleviates UC by modulating the gut microbiota and enhancing arginine biosynthesis.

The intricate relationship between human health and gut microecology has emerged as a central theme in contemporary medical research. Postmenopausal osteoporosis, primarily driven by estrogen deficiency, remains a major health concern. Traditional Chinese herbal medicines have attracted significant interest for their promising role in osteoporosis treatment.

The effects of Isaria felina, derived from Cordyceps sinensis, on postmenopausal osteoporosis in rats are the focus of this study. Adult female Sprague-Dawley rats were categorized into control, postmenopausal osteoporosis (OVX), and Isaria felina-treated (IF+OVX) groups. Following a 12-week treatment period, various analyses, including micro-CT, histological assessments, 16S rDNA sequencing, untargeted metabolomics, flow cytometry, and ELISA, were performed.

Micro-CT and histological assessments indicated significant improvements in bone loss and obesity control in OVX rats treated with Isaria felina. 16S rDNA sequencing revealed that Isaria felina corrected gut microbiota dysbiosis, particularly in the Bacteroides and Ruminococcus genera. Untargeted metabolomics highlighted alterations in nucleotide and lipid metabolism. Flow cytometry and ELISA analyses demonstrated that Isaria felina modulated the Th17/Treg immune balance, resulting in reduced levels of inflammatory cytokines IL-17 and TNF-α.

These findings indicate that Isaria felina mitigates bone loss in postmenopausal osteoporosis through modulation of gut microbiota and immune responses, underscoring its potential as a therapeutic agent for osteoporosis treatment.

Acute gastrointestinal injury (AGI) is known for its poor long-term prognosis and the associated increase in mortality among intensive care unit (ICU) patients. As the role of the gut microbiome and resistome in AGI remains unclear, the present study aimed to explore the possible associations between dysbacteriosis and in-hospital mortality in ICU patients with gastrointestinal dysfunction. Fecal samples were collected from a prospective cohort of 210 ICU patients with AGI, and shotgun metagenomic sequencing was used to determine the taxonomic composition of gut microbiota and the differences of antibiotic resistance genes (ARGs) between the Death and Survival groups. Compared to the Survival group, patients in the Death group shifted from strict anaerobes to facultative anaerobes in the fecal microbial community, with more Klebsiella but less Prevotella. The co-occurrence patterns revealed that more ARG subtypes were enriched in microbial taxa in the Death group, especially for Clostridium and Methanobrevibacter. Furthermore, the ARG type had large area under the curve (AUCs) in receiver operating characteristic for predicting the disease severity, and a combined gut microbiota-ARG subtype classifiers showed better performance than either of them. Thus, comparative metagenome-associated analysis can help to obtain valuable information about gut microbiota and gene coding for antibiotic resistance in AGI patients.

A metagenomic-related strategy was conducted to obtain a highly valuable resource to improve understanding of intestinal microbiota dysbiosis and antibiotic resistance genes (ARGs) profiles. The results indicate that intestinal microbiota, including Klebsiella and Prevotella, changed dramatically in intensive care unit (ICU) patients with acute gastrointestinal injury (AGI). Due to longer ICU stays and receiving more antibiotic treatment, the types and correlations of ARGs in the Death group were significantly higher than those in the Survival group. The findings of this study are expected to expand our knowledge of gut microbiota and resistome profiles reflecting gastrointestinal status, accelerate the identification of disease biomarkers, and provide new insights into the prevention and treatment of AGI-related diseases.

The Mediterranean diet (MD) is widely recognized for its health benefits, particularly in modulating gut microbiota composition and reducing the risk of metabolic, cardiovascular, and neurodegenerative diseases. Characterized by a high intake of plant-based foods, monounsaturated fats, and polyphenols, primarily from extra virgin olive oil, the MD fosters the growth of beneficial gut bacteria such as Bifidobacterium, Faecalibacterium prausnitzii, and Roseburia, which produce short-chain fatty acids that enhance gut barrier integrity, reduce inflammation, and improve metabolic homeostasis. Clinical and preclinical studies have proved that the MD is associated with increased microbial diversity, reduced pro-inflammatory bacteria, and improved markers of insulin sensitivity, lipid metabolism, and cognitive function. Additionally, the MD positively influences the gut microbiota in various conditions, including obesity, cardiovascular disease, and neurodegeneration, potentially mitigating systemic inflammation and enhancing neuroprotective mechanisms. Emerging evidence suggests that MD variants, such as the Green-MD, and their integration with probiotics can further optimize gut microbiota composition and metabolic parameters. While the beneficial impact of the MD on the gut microbiota and overall health is well supported, further long-term clinical trials are needed to better understand individual variability and improve dietary interventions tailored to different populations.

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent joint inflammation, damage, and loss of function. In recent years, the role of gut microbiota and its metabolites in immune regulation has attracted increasing attention. The gut microbiota influences the host immune system's homeostasis through various mechanisms, regulating the differentiation, function, and immune tolerance of immune cells. Dysbiosis of the gut microbiota in RA patients is closely associated with abnormal activation of immune cells and excessive secretion of inflammatory cytokines. Metabolites produced by the gut microbiota, such as short-chain fatty acids (SCFAs), tryptophan metabolites, bile acids, and amino acid metabolites, play a critical role in immune responses, regulating the functions of immune cells like T cells, B cells, and macrophages, and inhibiting the release of pro-inflammatory cytokines. Restoring the balance of the gut microbiota and optimizing the production of metabolic products may become a new strategy for RA treatment. This review discusses the role of gut microbiota and its metabolites in the immune response of RA, exploring how they influence the immunopathological process of RA through the regulation of immune cells and key immune factors. It also provides a theoretical basis for future therapeutic strategies based on gut microbiota modulation.

Multidrug-resistant bacteria are a clinical and an epidemiological challenge. However, the effects of multidrug-resistant bacteria and multi-antibiotic combination on gut microbiota are unclear. In this study, the effects of multidrug-resistant bacteria and multi-antibiotic combination on intestinal microbiota in mice have been observed by high-throughput sequencing. Resistant Escherichia coli (RP4) and 0.5, 1, and 2 mg/L antibiotics (Amp, Km, and Tet multi-antibiotic combination) could decrease the number of specific operational taxonomic units from 223 in the normal saline control group to 178 in the antibiotic-resistant bacteria group and 34 in the antibiotic group, and antibiotics are the biggest influencing factor. Multidrug-resistant bacteria and multi-antibiotic combination could affect the function of intestinal microbiota, and the effect of multidrug-resistant bacteria was similar to that of multi-antibiotic combination. Small intestine is the main colonization site of antibiotic-resistant bacteria, and Proteobacteria and Bacteroidetes are the major antibiotic-resistance acquired bacteria as determined by transmission electron microscopy and agarose plate screening culture.

Ruminants including goats have diverse microcosms of microbiota involved in diet digestion, absorption, and assimilation. Moreover, it is well known that changes in dietary regimens including nutrient levels result in varied gut microbiota composition, and ultimately, the performance and health of these animals.

The current study examined the effects of varying dietary energy and protein levels on the cecal fermentation, immune biomarkers, and microbiota characteristics of 80 male Yunshan Black Goats (6 months, ~35.82 ± 2.79 kg), divided into four diets: 1) High Energy-High Protein (HEHP), 2) High Energy-Low Protein (HELP), 3) Low Energy-High Protein (LEHP), and 4) Low Energy-Low Protein (LELP). Twenty goats (five from each treatment group) were randomly slaughtered after a 50-day feeding trial, and cecal digesta and tissue were sampled for microbial analysis.

The cecal content revealed that the high-energy groups (HEHP, HELP) had lower pH levels than the LEHP group (p < 0.05) and significantly higher valeric and isovaleric acid concentrations in HEHP. Although species richness (Chao1 index) remained consistent, the HEHP group showed higher diversity (Shannon and Simpson indices) than LEHP (p < 0.05). Dominant phyla included Bacteroidetes and Firmicutes; LEHP and LELP had significantly higher Bacteroidetes abundance than HELP, while HELP had higher Firmicutes abundance than LEHP (p < 0.05). Verrucomicrobia abundance was lower in LEHP than in HELP and LELP (p < 0.05). At the genus level, 311 genera were identified, with Clostridium, Prevotella, unidentified_BS11, and others showing significant variation. The HELP group had lower unidentified_BS11 than LEHP and LELP, and higher unidentified_Ruminococcaceae, Clostridium, and Lachnospiraceae than LEHP (p < 0.05). VFA metabolism, absorption, cytokine expression, and tight junction protein mRNA in cecal tissue were also analyzed. Genes like MCT-1 and SLC16A4, linked to VFA absorption, positively correlated with Paludibacter, which was associated with immune markers (TLR-3, TLR-4, IFN-γ) and Occludin expression. In contrast, VFA-related genes and tight junction proteins negatively correlated with unidentified Fibrobacterales, suggesting a microbial role in adaptive immunity.

This study demonstrated that dietary energy and protein levels significantly influenced cecal fermentation, immune biomarkers, and microbiota composition in Yunshan Black Goats.

Berberine is a promising agent for modulating the intestinal microbiota, playing a crucial role in human health homeostasis. This natural compound promotes the growth of beneficial bacteria such as Bacteroides, Bifidobacterium, and Lactobacillus while reducing harmful bacteria such as Escherichia coli. Clinical and preclinical studies demonstrate that Berberine helps regulate T2D and metabolic disorders, improves blood glucose levels during T2D, and reduces lipid profile and chronic inflammation, especially when combined with probiotics. Berberine represents a promising adjuvant therapy for inflammatory diseases, particularly intestinal disorders, due to its multifaceted actions of inhibiting proinflammatory cytokines and pathways during IBS, IBD, and UC and its modulation of gut microbiota and/or enhancement of the integrity of the intestinal epithelial barrier. This review establishes the basis for future treatment protocols with berberine and fully elucidates its mechanisms.

Ulcerative colitis (UC) remains an intractable and relapsing disease featured by intestinal inflammation. The anti-UC activity of Akkermansia muciniphila (AKK), an intestinal microorganism, has been widely investigated. The current work is to explore the impacts of AKK on UC and its possible reaction mechanism. In vivo UC model was induced by dextran sulfate sodium (DSS) and phorbol-12-myristate-13-acetate (PMA)-induced THP-1-M0 and raw264.7 macrophages were treated by lipopolysaccharide (LPS). H&E staining evaluated tissue damage. Inflammatory and oxidative stress levels were assessed by relevant kits. The high-throughput analysis of fatty acids was performed by the LC/MS method. RT-qPCR and Western blot detected related gene expression. Flow cytometry measured cell apoptosis and macrophage polarization. Energy metabolism was detected by ELISA, related assay kits, JC-1 staining, and Western blot. AKK reduced the pathological damage of mice colon tissues, alleviated oxidative stress and inflammatory response, upregulated the expression of Occludin-1 and SCFAs receptors, and stimulated M1 to M2 macrophage polarization in vivo. After FFAR2 was silenced, the promoting role of AKK in the viability and M1 to M2 macrophage polarization and the inhibitory role in oxidative stress, inflammation, apoptosis, energy metabolism disorder, necroptosis, and pyroptosis were both reverted. Conclusively, AKK might mediate SCFAs-SLC52A2/FFAR2 pathways to exert protective activities against intestinal inflammatory response in UC, suggesting that AKK might represent a novel and promising candidate for UC therapy.

Inflammation, oxidative stress, and metabolic diseases are intricately linked in a complex, self-reinforcing relationship. Inflammation can induce oxidative stress, while oxidative stress can trigger inflammatory responses, creating a cycle that contributes to the development and progression of metabolic disorders; in addition, these effects can be observed at systemic and local scales. Both processes lead to cellular damage, mitochondrial dysfunction, and insulin resistance, particularly affecting adipose tissue, the liver, muscles, and the gastrointestinal tract. This results in impaired metabolic function and energy production, contributing to conditions such as type 2 diabetes, obesity, and metabolic syndrome. Legumes are a good source of phenolic compounds and anthocyanins that exert an antioxidant effect-they directly neutralize reactive oxygen species and free radicals, reducing oxidative stress. In vivo, in vitro, and clinical trial studies demonstrate that these compounds can modulate key cellular signaling pathways involved in inflammation and metabolism, improving insulin sensitivity and regulating lipid and glucose metabolism. They also exert anti-inflammatory effects by inhibiting proinflammatory enzymes and cytokines. Additionally, anthocyanins and phenolics may positively influence the gut microbiome, indirectly affecting metabolism and inflammation.

Diabetes mellitus is a common chronic metabolic disease characterized by a high incidence and disability rate. Intestinal flora refers to the microbial community that lives in the intestines and plays a crucial role in maintaining intestinal health and the human immune system. In recent years, an increasing body of research has revealed a close relationship between intestinal flora and diabetes. The pathophysiological mechanisms between them have also been constantly uncovered, and the regulation of intestinal flora has shown promising efficacy in the adjuvant treatment of diabetes. This study mainly summarized the characteristics and mechanisms of intestinal flora in patients with diabetes in recent years, as well as the methods of regulating intestinal flora to prevent and treat diabetes, and prospected the future research direction. This will offer a theoretical basis for the clinical adjuvant treatment of diabetes with intestinal flora and the development of new drugs.

Atopic dermatitis (AD) is an allergic disease caused by various factors that can affect an individual's appearance and cause psychological stress. Therefore, it is necessary to investigate the underlying mechanisms and develop effective treatment strategies. The gut microbiota and bacterial metabolism play crucial roles in human diseases. However, their specific role in AD remains unclear.

In this study, we established a mouse model of AD and found that 2,4-dinitrofluorobenzene disrupted the skin barrier in mice. The species composition of intestinal bacteria was then analyzed by fecal 16s rRNA sequencing. The metabolic level of mice was analyzed by untargeted and targeted metabolomics in stool.

The levels of filaggrin and aquaporin 3 proteins in the model mice and total superoxide dismutase, catalase and malondialdehyde levels were significantly altered. Additionally, inflammatory factors such as tumor necrosis factor-alpha showed a significant increase. Using 16S rRNA gene sequencing, we identified 270 bacterial species with altered abundances of Ruminococcaceae and Bifidobacteriaceae. The untargeted metabolomic analysis detected 1,299 metabolites. Targeted analysis of free fatty acids revealed 49 metabolites with notable increases in linoleic and linolenic acid levels. Fecal bacterial transplantation experiments have demonstrated that oxidative stress, inflammation, and skin barrier damage were alleviated after transplantation.

These findings suggested that the metabolite linoleic acid negatively correlated with Ruminococcaceae and Bifidobacteriaceae may influence AD development. Perturbations in the intestinal bacteria and flora contributed to the development of AD, and the mouse model could serve as a valuable tool for further investigation of therapeutic approaches for managing ADS.

This research aimed to probe the effects of fecal microbiota and Lactobacillus acidophilus on the metabolism of Radix Astragali (RA) and Poria cocos solid fermenting Radix Astragali (FRA). It further explores pharmacological effects of RA, Poria cocos, and FRA on HUA mouse model and the mechanisms in HUA treatment.

Fecal microbiota and Lactobacillus acidophilus were used to ferment FRA and RA in vitro to probe the impacts of microbiota on the metabolism of active compound. A HUA mouse model was used to carry out pharmacodynamic experiment of anti-hyperuricemia. Network pharmacology and molecular docking was utilized to elucidate the underlying mechanisms of RA and Poria cocos in the treatment of HUA.

The results indicated that astragaloside IV (AG IV), total saponins, and flavonoids continuously decreased in FRA and RA during 48 h fecal microbiota colonic fermentation. During Lactobacillus acidophilus fermentation, in FRA, the content of AG IV peaked at 12 h with a value of 1.14 ± 0.20 mg/g; total saponins and flavonoids reached the highest values of 136.34 ± 6.15 mg/g at 12 h and 6.35 ± 0.06 mg/g at 6 h; AG IV and total saponins reached the highest values 0.63 ± 0.05 mg/g and 115.12 ± 4.12 mg/g at 12 h and 24 h in RA, respectively; and total flavonoids consecutively decreased. The counts of Lactobacillus acidophilus increased significantly in FRA compared with RA. Pharmacodynamic outcomes revealed that FRA effectively reduced blood levels of uric acid (UA), triglycerides (TG), xanthine oxidase (XOD), alanine aminotransferase (ALT), and aspartate transaminase (AST) in HUA mice, exerting protective effects on the liver and kidney. Network pharmacology showed that there were 93 common targets for RA, Poria cocos, and HUA with the top five core targets tumor necrosis factor (TNF), signal transducer and activator of transcription 3 (STAT3), cysteinyl aspartate specific proteinase 3 (CASP3), jun proto-oncogene (JUN), and estrogen receptor 1 (ESR1). Molecular docking analysis revealed that AG IV, calycosin and formononetin bond well to the core targets.

This research revealed the interaction of RA and FRA with fecal microbiota and Lactobacillus acidophilus, RA and Poria cocos were featured with multiple components, target points, and signaling pathways in HUA treatment, which provided fresh insights for further HUA therapeutics.

Intestinal tract is the largest immune system of human body. Gut microbiota (GM) can produce a large number of metabolites, such as short-chain fatty acids and bile acids, which regulate the physiological health of the host and affect the development of disease. In recent years, traditional Chinese medicine (TCM) polysaccharides have attracted extensive attention with multiple biological activities and low toxicity. TCM polysaccharides can promote the growth of intestinal beneficial bacteria and inhibit the growth of harmful bacteria by regulating the structure and function of GM, thus playing a crucial role in preventing or treating chronic diseases such as inflammatory bowel disease (IBD), obesity, type 2 diabetes mellitus (T2DM), liver diseases, cancer, etc. In this paper, the research progress of TCM polysaccharides in the treatment of chronic diseases such as inflammatory bowel disease, obesity, T2DM, liver diseases, cancer, etc. by modulating GM was reviewed. Meanwhile, this review makes an in-depth discussion on the shortcomings of the research of TCM polysaccharides on chronic diseases by modulating GM, and new valuable prospection for the future researches of TCM polysaccharides are proposed, which will provide new ideas for the further study of TCM polysaccharides.

The global epidemic of type 2 diabetes mellitus (T2DM) imposes a substantial burden on public health and healthcare expenditures, thereby driving the pursuit of cost-effective preventive and therapeutic strategies. Emerging evidence suggests a potential association between dysbiosis of gut microbiota and its metabolites with T2DM, indicating that targeted interventions aimed at modulating gut microbiota may represent a promising therapeutic approach for the management of T2DM. In this review, we concentrated on the multifaceted interactions between the gut microbiota and the intestinal barrier in the context of T2DM. We systematically summarized that the imbalance of beneficial gut microbiota and its metabolites may constitute a viable therapeutic approach for the management of T2DM. Meanwhile, the mechanisms by which gut microbiota interventions, such as probiotics, prebiotics, postbiotics, and synbiotics, synergistically improve insulin resistance in T2DM are summarized. These mechanisms include the restoration of gut microbiota structure, upregulation of intestinal epithelial cell proliferation and differentiation, enhancement of tight junction protein expression, promotion of mucin secretion by goblet cells, and the immunosuppressive functions of regulatory T cells (Treg) and M2 macrophages. Collectively, these actions contribute to the amelioration of the body's metabolic inflammatory status. Our objective is to furnish evidence that supports the clinical application of probiotics, prebiotics, and postbiotics in the management of T2DM.

Fusobacterium nucleatum (F. nucleatum), an anaerobic resident of the oral cavity, is increasingly recognized as a contributing factor to ulcerative colitis (UC). The adhesive properties of F. nucleatum are mediated by its key virulence protein, FadA adhesin. However, further investigations are needed to understand the pathogenic mechanisms of this oral pathogen in UC. The present study aimed to explore the role of the FadA adhesin in the colonization and invasion of oral F. nucleatum in dextran sulphate sodium (DSS)-induced colitis mice via molecular techniques. In this study, we found that oral inoculation of F. nucleatum strain carrying the FadA adhesin further exacerbated DSS-induced colitis, leading to elevated alveolar bone loss, disease severity, and mortality. Additionally, CDH1 gene knockout mice treated with DSS presented increases in body weight and alveolar bone density, as well as a reduction in disease severity. Furthermore, FadA adhesin adhered to its mucosal receptor E-cadherin, leading to the phosphorylation of β-catenin and the degradation of IκBα, the activation of the NF-κB signalling pathway and the upregulation of downstream cytokines. In conclusion, this research revealed that oral inoculation with F. nucleatum facilitates experimental colitis via the secretion of the virulence adhesin FadA. Targeting the oral pathogen F. nucleatum and its virulence factor FadA may represent a promising therapeutic approach for a portion of UC patients.

Grifola frondosa polysaccharide (GFP) is a consumable fungus recognized for its potential health advantages. The present study aimed to investigate the development and potential etiologies of ulcerative colitis (UC) utilizing oxazolone (OXZ) as an inducer in mice, along with assessing the therapeutic effects of GFP at varying doses in UC mice, with sulfasalazine (SASP) serving as the positive control. The obtained results indicated that OXZ intervention in mice induced numerous physical manifestations of UC, including increased disease activity index (DAI), decreased goblet cell division, enhanced fibrosis, reduced expression of Claudin1 and Zona encludens protein1 (ZO-1), decreased proliferative activity of colonic mucosal epithelial cells, disturbed oxidation balance, and alterations in intestinal flora. Nonetheless, GFP intervention significantly ameliorated or even resolved these abnormal indicators to a considerable extent. Consequently, this study suggests that GFP might serve as a prebiotic to regulate intestinal flora, mitigate enterotoxin production, restore oxidative balance, thereby reducing the generation of inflammatory mediators, restoring the intestinal barrier, and ultimately improving OXZ-induced UC in mice. GFP demonstrates promising potential as a candidate drug for colitis treatment and as a dietary supplement for alleviating intestinal inflammatory issues.

The gut microbiome (GM), often referred to as the second genome of the human body, plays a crucial role in various metabolic processes and mediates the development of numerous diseases. Intervertebral disc degeneration (IDD) is an age-related degenerative spinal disease characterized by the loss of disc height, hydration, and integrity, leading to pain and reduced mobility. Although the pathogenesis of IDD is not fully understood, recent studies suggest that dysbiosis of the gut microbiome may accelerate the progression of IDD through multiple mechanisms. This article begins by discussing the potential relationship between GM dysbiosis and human diseases, followed by a comprehensive review of the regulatory mechanisms of GM in skeletal diseases within the gut-disc axis framework. Furthermore, it explores three potential pathways through which GM dysbiosis may mediate the development of IDD: immunomodulation, bacterial translocation and colonization, and the decomposition and absorption of intestinal metabolites. These pathways can disrupt disc cell homeostasis and promote degenerative changes. Finally, this paper summarizes for the first time the potential therapeutic approaches for delaying IDD by targeting the gut-disc axis, providing new insights into the pathogenesis and regenerative repair strategies for IDD.

Patients with gastrointestinal (GI) disorders might benefit from probiotic supplementation to resolve their bowel symptoms and enhance their quality of life (QoL). This systematic review aimed to evaluate the effects of oral probiotic supplementation on improving QoL. Relevant studies were systematically searched in online databases, including PubMed, Scopus, Embase, ProQuest, and Google Scholar up to September 2022 using relevant keywords. Studies that were conducted on GI patients and presented QoL outcomes were included. The Revised Cochrane Risk of Bias 2 tool and the Risk Of Bias In Non-randomized Studies of Intervention tool were used to assess the risk of bias. Of the 4,555 results found in the systematic search of databases, only 36 studies were eligible for evaluation. According to this systematic review, 24 studies reported improvements, whereas 12 studies reported no improvements on QoL in GI patients supplemented with probiotics. We found that probiotics may improve the QoL of patients with GI diseases and related metabolic complications. Therefore, probiotics can be a useful supportive treatment strategy in these patients.

Intestinal microbiota and its metabolites are involved in many physiological processes of the human body and play a vital role in maintaining human health. The occurrence of kidney disease can cause intestinal microbiota imbalance, resulting in diarrhea. The change of intestinal microbiota and its metabolites content can aggravate renal function injury, which has a bidirectional regulating effect. The theory of renal-intestinal axis further clarified that the impaired renal function is related to the imbalance of intestinal microorganisms, and the impaired intestinal barrier is related to the accumulation of toxin products. Because of its unique therapeutic advantages, Traditional Chinese Medicine can treat diarrhea by enhancing the growth of beneficial bacteria, inhibiting pathogenic bacteria and immune regulation, and slow down the continuous deterioration of kidney disease. This paper focuses on the relationship between intestinal microbiota and its metabolites and diarrhea, the influence of Traditional Chinese Medicine on intestinal microbiota in the treatment of diarrhea, and the role of intestinal microbiota and its metabolites in the renal-intestinal axis. It provides a theoretical basis for Traditional Chinese Medicine to regulate intestinal microbiota and its metabolites based on the renal-intestinal axis theory to treat nephrology-induced diarrhea, and also provides a new idea and method for Traitional Chinese Medicine to treat nephrology-induced diarrhea.

Maintaining a healthy intestinal environment, optimal epithelial barrier integrity, and balanced gut microbiota composition are essential for the growth performance of weaning pigs. We identified Lactiplantibacillus argentoratensis AGMB00912 (LA) in healthy porcine feces as having antimicrobial activity against pathogens and enhanced short-chain fatty acid (SCFA) production. Herein, we assess the protective role of LA using a weaning mouse model with enterotoxigenic Escherichia coli (ETEC) infection. LA treatment improves feed intake and weight gain and alleviates colon shortening. Furthermore, LA inhibits intestinal damage, increases the small intestine villus height compared with the ETEC group, and enhances SCFA production. Using the Kyoto Encyclopedia of Genes and Genomes and other bioinformatic tools, including InterProScan and COGNIZER, we validated the presence of SCFA-producing pathways of LA and Lactiplantibacillus after whole genome sequencing. LA mitigates ETEC-induced shifts in the gut microbiota, decreasing the proportion of Escherichia and Enterococcus and increasing SCFA-producing bacteria, including Kineothrix, Lachnoclostridium, Roseuburia, Lacrimispora, Jutongia, and Blautia. Metabolic functional prediction analysis revealed enhanced functions linked to carbohydrate, amino acid, and vitamin biosynthesis, along with decreased functions associated with infectious bacterial diseases compared to the ETEC group. LA mitigates the adverse effects of ETEC infection in weaning mice, enhances growth performance and intestinal integrity, rebalances gut microbiota, and promotes beneficial metabolic functions. These findings validate the functionality of LA in a small animal model, supporting its potential application in improving the health and growth performance of weaning pigs.

This manuscript provides an overview of the microbiota profile associated with precancerous lesions in the esophagus, stomach, and large bowel. The critical review of the available data reveals significant variability in the methods used for microbiota profiling. This variability may affect the reliable identification of specific biological links between histologically profiled neoplastic diseases and the microbiota population. Overall, this critical review reveals significant links between microbiota communities and the different lesions within the spectrum of the oncogenetic cascade in various epidemiological contexts and anatomical districts.

Non-small cell lung cancer (NSCLC) patients undergoing chemotherapy and immunotherapy experience disturbances in the gut microbiota. This study intends to find out the correlation between gut microbiota and clinical indices before and after radiotherapy for NSCLC.

Ten patients with primary NSCLC were screened, and plasma and fecal samples were collected before and after radiotherapy, respectively. Inflammatory indices in plasma were detected. Genomic DNA was extracted from fecal specimens and sequenced on on Illumina HiSeq2000 sequencing platform. Thee sequenced data were subjected to Metagenome assembly, gene prediction, species annotation, and gene function analysis to study and analyze gut microbiota and metabolic functions. The correlation between the diversity of gut microbiota and the clinical indicators of NSCLC patients was evaluated, and the changes of gut microbiota before and after radiotherapy were observed.

The diversity of gut microbiota in NSCLC patients did not correlate with smoking, pathology, and inflammatory markers. The abundance of phylum (p)_Bacteroidetes increased; p_Firmicutes and p_Bacteroidetes accounted for the highest proportion in NSCLC patients, and the abundance of both was dominantly exchanged after radiotherapy. There was a decrease in genus (g)_Bifidobacterium after radiotherapy in NSCLC patients. There was no significant correlation between the diversity of gut microbiota after radiotherapy and radiotherapy sensitivity, and the structural composition and abundance of gut microbiota remained stable.

The diversity of gut microbiota is altered after radiotherapy in NSCLC patients, showing an increase in harmful bacteria and a decrease in beneficial bacteria.

Since the first published case study of human intestinal transplantation in 1967, there have been significant studies of intestinal transplant immunology in both animal models and humans. An improved understanding of the profiles of different immune cell subsets is critical for understanding their contributions to graft outcomes. While different studies have focused on the contribution of one or a few subsets to intestinal transplant, no study has integrated these data for a comprehensive overview of immune dynamics after intestinal transplant. Here, we provide a systematic review of the literature on different immune subsets and discuss their roles in intestinal transplant outcomes on multiple levels, focusing on chimerism and graft immune reconstitution, clonal alloreactivity, and cell phenotype. In Sections 1, 2 and 3, we lay out a shared framework for understanding intestinal transplant, focusing on the mechanisms of rejection or tolerance in the context of mucosal immunology and illustrate the unique role of the bidirectional graft-versus-host (GvH) and host-versus-graft (HvG) alloresponse. In Sections 4, 5 and 6, we further expand upon these concepts as we discuss the contribution of different cell subsets to intestinal transplant. An improved understanding of intestinal transplantation immunology will bring us closer to maximizing the potential of this important treatment.

Helicobacter pylori (H. pylori) infection presents increasing challenges to antibiotic therapies in limited penetration through gastric mucus, multi-drug resistance (MDR), biofilm formation, and intestinal microflora dysbiosis. To address these problems, herein, a mucus-penetrating phototherapeutic nanomedicine (RLs@T780TG) against MDR H. pylori infection is engineered. The RLs@T780TG is assembled with a near-infrared photosensitizer T780T-Gu and an anionic component rhamnolipids (RLs) for deep mucus penetration and light-induced anti-H. pylori performances. With optimized suitable size, hydrophilicity and weak negative surface, the RLs@T780TG can effectively penetrate through the gastric mucus layer and target the inflammatory site. Subsequently, under irradiation, the structure of RLs@T780TG is disrupted and facilitates the T780T-Gu releasing to target the H. pylori surface and ablate multi-drug resistant (MDR) H. pylori. In vivo, RLs@T780TG phototherapy exhibits impressive eradication against H. pylori. The gastric lesions are significantly alleviated and intestinal bacteria balance is less affected than antibiotic treatment. Summarily, this work provides a potential nanomedicine design to facilitate in vivo phototherapy in treatment of H. pylori infection.

Paraprobiotics and postbiotics have shown potential in the treatment of ulcerative colitis (UC). However, their in vivo application is still in its infancy and their mechanisms of action are not well understood.

Here, we investigated the mitigation effects of Limosilactobacillus fermentum HF06-derived paraprobiotic (6-PA) and postbiotic (6-PS) on dextran sulfate sodium induced UC and the potential mechanisms. Results indicated that the administration of 6-PA and 6-PS resulted in the inhibition of weight loss and colon shortening in mice with UC. Furthermore, they led to a significant reduction in both fecal moisture content and the levels of proinflammatory cytokines and oxidative stress in the intestine of the mice. 6-PA and 6-PS treatment strengthened the intestinal mucosal barrier by dramatically upregulating the levels of zonula occludens-1 and occludin proteins. In addition, 6-PA and 6-PS restored intestinal dysbiosis by regulating abundances of certain bacteria, such as Bifidobacterium, Faecalibaculum, Muribaculaceae, Corynebacterium, Escherichia-Shigella and Clostridium_sensu_stricto_1, and regulated the level of short-chain fatty acids.

These findings illustrated for the first time that L. fermentum HF06-derived paraprobiotic and postbiotic enhanced the intestinal barrier function, and restored gut microbiota alterations. © 2023 Society of Chemical Industry.

Ulcerative colitis (UC) is an intestinal disease that is becoming increasingly prevalent and is often overlooked in early stages, and its pathogenesis is often closely related to inflammatory processes. Betaine is a natural product with anti-inflammatory effects that exists in a wide range of plants and animals.

In this study, the protective effects of betaine are investigated on intestinal barrier function in a mouse model, a dextran sulfate sodium-induced ulcerative colitis and its mechanism of action in the inflammatory context. FITC-dextran 4000 Da (FD-4) flux, disease activity index, histopathological scores, and inflammatory factor levels in sera are determined across different groups. In addition, Caco-2 cell monolayer barrier function is evaluated by transepithelial resistance and FD-4 flux. The expression levels and distribution of tight junction proteins are determined using Western blot and immunofluorescence, respectively. Activation of the NF-κBp65/MLCK/p-MLC signaling pathway is detected by Western blot. Chromatin immunoprecipitation is performed to examine the binding of NF-κB to the MLCK gene promoter. The results indicated that betaine inhibits NF-κB-mediated activation of the MLCK/p-MLC signaling pathway to protect the intestinal barrier function of mice with UC.

Betaine can be used as a potential candidate drug to improve intestinal barrier dysfunction in patients with UC.

Peutz-Jeghers Syndromeis a rare autosomal dominant genetic disease characterized by gastrointestinal hamartomatous polyps and skin and mucous membrane pigmentation. The pathogenesis of PJS remains unclear; however, it may be associated with mutations in the STK11 gene, and there is currently no effective treatment available. The gut microbiota plays an important role in maintaining intestinal homeostasis in the human body, and an increasing number of studies have reported a relationship between gut microbiota and human health and disease. However, relatively few studies have been conducted on the gut microbiota characteristics of patients with PJS. In this study, we analyzed the characteristics of the gut microbiota of 79 patients with PJS using 16 S sequencing and measured the levels of short-chain fatty acids in the intestines. The results showed dysbiosis in the gut microbiota of patients with PJS, and decreased synthesis of short-chain fatty acids. Bacteroides was positively correlated with maximum polyp length, while Agathobacter was negatively correlated with age of onset. In addition, acetic acid, propionic acid, and butyric acid were positively correlated with the age of onset but negatively correlated with the number of polyps. Furthermore, the butyric acid level was negatively correlated with the frequency of endoscopic surgeries. In contrast, we compared the gut microbiota of STK11-positive and STK11-negative patients with PJS for the first time, but 16 S sequencing analysis revealed no significant differences. Finally, we established a random forest prediction model based on the gut microbiota characteristics of patients to provide a basis for the targeted diagnosis and treatment of PJS in the future.

Colorectal cancer (CRC) is the third most common cancer in the world, and its incidence rate and mortality are on the rise in many countries. In recent years, with the improvement of economic conditions, people's living habits have changed, including lack of physical activity, poor diet patterns and circadian rhythm disorder. These risk factors can change the colon environment and the composition of intestinal microbiota. This state is called intestinal imbalance, which increases the risk of cancer. Probiotics, a class of microorganisms that help maintain gut microbial homeostasis and alleviate dysbiosis, may help prevent inflammation and colorectal cancer. These probiotics inhibit or ameliorate the effects of dysbiosis through the production of short-chain fatty acids (SCFAs), modulation of immunity, maintenance of the intestinal epithelial barrier, pro-apoptotic mechanisms, and other mechanisms. This review aims to explain the interaction between probiotics, the gut microenvironment and the gut microbiota, and summarize reports on the possibility of probiotics in the prevention and treatment of colorectal cancer.

The gut microbiota consists of a set of microorganisms that colonizes the intestine and ferment fibers, among other nutrients, from the host's diet. A healthy gut microbiota, colonized mainly by beneficial microorganisms, has a positive effect on digestion and plays a role in disease prevention. However, dysregulation of the gut microbiota can contribute to various diseases. The nutrition of the host plays an important role in determining the composition of the gut microbiota. A healthy diet, rich in fiber, can beneficially modulate the gut microbiota. In this sense, oats are a source of both soluble and insoluble fiber. Oats are considered a functional ingredient with prebiotic potential and contain plant proteins, unsaturated fats, and antioxidant compounds. The impact of oat consumption on the gut microbiota is still emerging. Associations between oat consumption and the abundance of Akkermansia muciniphila, Roseburia, Lactobacillus, Bifidobacterium, and Faecalibacterium prausnitzii have already been observed. Therefore, this integrative review summarizes the findings from studies on the relationship between oat consumption, the gut microbiota, and the metabolites, mainly short-chain fatty acids, it produces.

Gut microbiota influence food allergy. We showed that the natural compound berberine reduces IgE and others reported that BBR alters gut microbiota implying a potential role for microbiota changes in BBR function.

We sought to evaluate an oral Berberine-containing natural medicine with a boiled peanut oral immunotherapy (BNP) regimen as a treatment for food allergy using a murine model and to explore the correlation of treatment-induced changes in gut microbiota with therapeutic outcomes.

Peanut-allergic (PA) mice, orally sensitized with roasted peanut and cholera toxin, received oral BNP or control treatments. PA mice received periodic post-therapy roasted peanut exposures. Anaphylaxis was assessed by visualization of symptoms and measurement of body temperature. Histamine and serum peanut-specific IgE levels were measured by ELISA. Splenic IgE+B cells were assessed by flow cytometry. Fecal pellets were used for sequencing of bacterial 16S rDNA by Illumina MiSeq. Sequencing data were analyzed using built-in analysis platforms.

BNP treatment regimen induced long-term tolerance to peanut accompanied by profound and sustained reduction of IgE, symptom scores, plasma histamine, body temperature, and number of IgE+ B cells (p <0.001 vs Sham for all). Significant differences were observed for Firmicutes/Bacteroidetes ratio across treatment groups. Bacterial genera positively correlated with post-challenge histamine and PN-IgE included Lachnospiraceae, Ruminococcaceae, and Hydrogenanaerobacterium (all Firmicutes) while Verrucromicrobiacea. Caproiciproducens, Enterobacteriaceae, and Bacteroidales were negatively correlated.

BNP is a promising regimen for food allergy treatment and its benefits in a murine model are associated with a distinct microbiota signature.

Dietary plant polysaccharides, one of the main sources of natural polysaccharides, possess significant cancer prevention activity and potential development value in the food and medicine fields. The anti-tumor mechanisms of plant polysaccharides are mainly elaborated from three perspectives: enhancing immunoregulation, inhibiting tumor cell growth and inhibiting tumor cell invasion and metastasis. The immune system plays a key role in cancer progression, and immunomodulation is considered a significant pathway for cancer prevention or treatment. Although much progress has been made in revealing the relationship between the cancer prevention activity of polysaccharides and immunoregulation, huge challenges are still met in the research and development of polysaccharides. Results suggest that certain polysaccharide types and glycosidic linkage forms significantly affect the biological activity of polysaccharides in immunoregulation. At present, the in vitro anti-tumor effects and immunoregulation of dietary polysaccharides are widely reported in articles; however, the anti-tumor effects and in vivo immunoregulation of dietary polysaccharides are still deserving of further investigation. In this paper, aspects of the mechanisms behind dietary polysaccharides' cancer prevention activity achieved through immunoregulation, the role of immune cells in cancer progression, the role of the mediatory relationship between the gut microbiota and dietary polysaccharides in immunoregulation and cancer prevention are systematically summarized, with the aim of encouraging future research on the use of dietary polysaccharides for cancer prevention.

Heart failure (HF) is the terminal stage of multiple cardiovascular diseases, with high mortality and morbidity. More and more studies have proved that gut microbiota may play a role in the process of HF, which is expected to become a new therapeutic target. The combination of traditional Chinese and Western medicine has vast therapeutic potential of complementation against HF.

This manuscript expounds on the research progress of mechanisms of gut microbiota participating in the occurrence and prognosis of HF and the role of integrative traditional Chinese and Western medicine from 1987 to 2022. The combination of traditional Chinese and Western medicine in the prevention and treatment of HF from the perspective of gut microbiota has been discussed.

Studies focusing on the effects and their mechanisms of gut microbiota in HF and the role of integrative traditional Chinese and Western medicine were identified and summarized, including contributions from February 1987 until August 2022. The investigation was carried out in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) guidelines. We searched PubMed, Embase, Cochrane Library, CNKI, Wanfang, and VIP databases up to April 2023 by using the relevant keywords and operators.

A total of 34 articles were finally included in this review.16 RCTs and 13 basic researches, and 3 clinical research studies involving 7 relevant outcome indicators(cardiac function evaluation index, changes in gut microbiota, inflammatory factors, metabolites of gut microbiota, serum nutritional index protein, quality of life score, intestinal permeability and all-cause mortality). Compared with healthy controls, serum TNF-α and TMAO levels were significantly higher in patients with heart failure [MD = 5.77, 95%CI(4.97, 6.56), p < 0.0001; SMD = 1.92, 95%CI(1.70, 2.14), p < 0.0001]. Escherichia coli and Thick-walled bacteria increased significantly [SMD = -0.99, 95%CI(-1.38, -0.61), p < 0.0001, SMD = 2.58, 95%CI(2.23, 2.93), p < 0.0001];The number of bacteroides and lactobacillus decreased [SMD = -2.29, 95%CI(-2.54, -2.04), p < 0.0001; SMD = -1.55, 95%CI(-1.8, -1.3), p < 0.0001]. There was no difference in bifidobacterium [SMD = 0.16, 95%CI(-0.22, 0.54), p = 0.42]. In the published literature, it is not difficult to see that most of the results are studied and proved based on animal experiments or clinical trials, involving the cellular level, while the mechanism and mode of action of the molecular biology of traditional Chinese medicine are less elaborated, which is related to the characteristics of multi-components and multi-targets of traditional Chinese medicine. The above are the shortcomings of published literature, which can also be the direction of future research.

Heart failure patients have decreased beneficial bacteria such as Bacillus mimics and Lactobacillus in the intestinal flora and increased harmful flora like thick-walled flora. And increase the inflammatory response of the body and the expression of trimethylamine oxide (TMAO) in the serum. And The prevention and treatment of integrative traditional Chinese and Western medicine against heart failure based on gut microbiota and its metabolites is a promising research direction.

The maintenance of redox homeostasis is associated with a healthy status while the disruption of this mechanism leads to the development of various pathological conditions. Bioactive molecules such as carbohydrates accessible to the microbiota (MACs), polyphenols, and polyunsaturated fatty acids (PUFAs) are food components best characterized for their beneficial effect on human health. In particular, increasing evidence suggests that their antioxidant ability is involved in the prevention of several human diseases. Some experimental data indicate that the activation of the nuclear factor 2-related erythroid 2 (Nrf2) pathway-the key mechanism in the maintenance of redox homeostasis-is involved in the beneficial effects exerted by the intake of PUFAs and polyphenols. However, it is known that the latter must be metabolized before becoming active and that the intestinal microbiota play a key role in the biotransformation of some ingested food components. In addition, recent studies, indicating the efficacy of the MACs, polyphenols, and PUFAs in increasing the microbial population with the ability to yield biologically active metabolites (e.g., polyphenol metabolites, short-chain fatty acids (SCFAs)), support the hypothesis that these factors are responsible for the antioxidant action on the physiology of the host. The underlying mechanisms through which MACs, polyphenols, and PUFAs might influence the redox status have not been fully elucidated, but based on the efficacy of SCFAs as Nrf2 activators, their contribution to the antioxidant efficacy of dietary bioactives cannot be excluded. In this review, we aimed to summarize the main mechanisms through which MACs, polyphenols, and PUFAs can modulate the host's redox homeostasis through their ability to directly or indirectly activate the Nrf2 pathway. We discuss their probiotic effects and the role played by the alteration of the metabolism/composition of the gut microbiota in the generation of potential Nrf2-ligands (e.g., SCFAs) in the host's redox homeostasis.

This study aimed to clarify the characteristics of intestinal microbiota in children with hand, foot, and mouth disease (HFMD) under 3 years old. Fresh feces were collected from 54 children with HFMD and 30 healthy children. All of them were <3 years old. Sequencing of the 16S rDNA amplicons was performed. Between the 2 groups, the richness, diversity, and structure of the intestinal microbiota were analyzed by α-diversity and β-diversity. Linear discriminant analysis and LEfSe analyses were used to compare different bacterial classifications. The sex and age of the children in the 2 groups were not statistically significant (P = .92 and P = .98, respectively). Compared to healthy children, the Shannon index, Ace index, and Chao index were lower in children with HFMD (P = .027, P = .012, and P = .012, respectively). Based on the weighted or unweighted UniFrac distance analysis, the structure of the intestinal microbiota in HFMD was also significantly changed (P = .002 and P < .001, respectively). Linear discriminant analysis and LEfSe analysis showed that the changes of key bacteria were manifested as a decrease in Prevotella and Clostridium_XIVa (P < .001 and P < .001, respectively), while Escherichia and Bifidobacterium increased (P = .025 and P = .001, respectively). Children with HFMD under 3 years of age have intestinal microbiota disorder and show a decrease in diversity and richness. The decrease in the abundance of Prevotella and Clostridium, which can produce short-chain fatty acids, is also one of the characteristics of the change. These results can offer a theoretical foundation for the pathogenesis and microecological treatment of HFMD in infants.

Esophageal cancer is a major health problem, being the seventh most incidence cancer worldwide. Due to the often-late diagnosis and lack of efficient treatments, the overall 5-year survival is as low as 10%. Therefore, understanding the etiology and the mechanisms that drive the development of this type of cancer could improve the management of patients, increasing the chance of achieving a better clinical outcome. Recently, the microbiome has been studied as a putative etiological factor for esophageal cancer. Nevertheless, the number of studies tackling this issue is low, and the heterogeneity in the study design and data analysis has hindered consistent findings. In this work, we reviewed the current literature on the evaluation of the role of microbiota in the development of esophageal cancer. We analyzed the composition of the normal microbiota and the alterations found in precursor lesions, namely Barrett's esophagus and dysplasia, as well as in esophageal cancer. Additionally, we explored how other environmental factors can modify microbiota and contribute to the development of this neoplasia. Finally, we identify critical aspects to be improved in future studies, with the aim of refining the interpretation of the relationship between the microbiome and esophageal cancer.

Enterotoxigenic Escherichia coli (ETEC) causing post-weaning diarrhea (PWD) in piglets have a detrimental impact on animal health and economy in pig production. ETEC strains can adhere to the host's small intestinal epithelial cells using fimbriae such as F4 and F18. Phage therapy could represent an interesting alternative to antimicrobial resistance against ETEC infections. In this study, four bacteriophages, named vB_EcoS_ULIM2, vB_EcoM_ULIM3, vB_EcoM_ULIM8 and vB_EcoM_ULIM9, were isolated against an O8:F18 E. coli strain (A-I-210) and selected based on their host range. These phages were characterized in vitro, showing a lytic activity over a pH (4-10) and temperature (25-45 °C) range. According to genomic analysis, these bacteriophages belong to the Caudoviricetes class. No gene related to lysogeny was identified. The in vivo Galleria mellonella larvae model suggested the therapeutic potential of one selected phage, vB_EcoS_ULIM2, with a statistically significant increase in survival compared to non-treated larvae. To assess the effect of this phage on the piglet gut microbiota, vB_EcoS_ULIM2 was inoculated in a static model simulating the piglet intestinal microbial ecosystem for 72 h. This study shows that this phage replicates efficiently both in vitro and in vivo in a Galleria mellonella model and reveals the safety of the phage-based treatment on the piglet microbiota.

Food allergies can cause intestinal damage that can exacerbate allergic symptoms, and gut microbiota have been shown to influence allergic development. This study was intended to investigate the effects of Avenanthramide (AVA) on colonic damage induced by food allergy and its mechanism. In Exp. 1, AVA administrations alleviated colonic inflammation in mice challenged with ovalbumin, as shown by decreased concentrations of TNF-α, IL-25 and IL-33. Additionally, the AVA supplementations improved intestinal barrier damage by elevating occludin, ZO-1 and claudin-1 levels. Moreover, AVA inhibited NF-κB phosphorylation and enhanced heat shock protein 70 (Hsp70) expression in the colon. In Exp. 2, apoptozole as a Hsp70 inhibitor was used to explore the Hsp70-NF-κB signaling contribution to AVA function. The AVA additions increased the productions of acetate and butyrate, but decreased propionate. Notably, AVA reduced the colonic abundance of propionate-producing microbes such as Muribaculaceae, but elevated butyrate-producing microbes including Roseburia, Blautia, and Lachnospiraceae_NK4A136_group. Microbial alteration could be responsible for the increased butyrate, and thus the up-regulated Hsp70. However, apoptozole treatment eliminated the effects of AVA. Our study revealed that AVA improved colonic injury and inflammation induced by food allergies, and this mechanism may be mediated by the increased microbial-derived butyrate and involved in the Hsp70-NF-κB signaling.