Immune system function is intricately shaped by nutritional status, dietary patterns, and gut microbiota composition. Micronutrients such as vitamins A, C, D, E, B-complex, zinc, selenium, iron, and magnesium are critical for maintaining physical barriers, supporting immune cell proliferation, and regulating inflammation. Macronutrients-including proteins, fats, and carbohydrates-also modulate immune responses through their impact on immune metabolism and the gut-immune axis. Epigenetic mechanisms, including DNA methylation, histone modifications, and microRNA expression, mediate the long-term effects of diet on immune function and tolerance. Diet-induced alterations in gut microbiota further influence immune homeostasis via microbial metabolites like short-chain fatty acids. Imbalanced diets, particularly the Western diet, contribute to immune dysregulation, chronic inflammation, and the development of metabolic disorders such as obesity and type 2 diabetes. While plant-based and Mediterranean dietary patterns have shown anti-inflammatory and immunoregulatory benefits, gaps remain in understanding the long-term epigenetic impacts of these diets. This review integrates current knowledge on how nutrition and the microbiome regulate immunity, highlighting future directions for personalized dietary strategies in preventing chronic immune-related conditions.

Patients with inflammatory bowel diseases (IBDs) are at risk of protein malnutrition due to increased protein loss or reduced dietary intake. The consequences of protein malnutrition on intestinal epithelial metabolism and disease progression remain poorly understood.

Given the critical role of the mechanistic target of rapamycin complex 1 (mTORC1) as an amino acid sensor and a key regulator of intestinal epithelial metabolism and homeostasis, along with the well-established influence of diet on the gut microbiota and IBD, we focused on accessing the role of dietary protein in modulating intestinal epithelial mTORC1, determine the contributions of specific amino acids such as leucine and arginine, and examine the interplay between protein malnutrition and gut microbiota driving IBD.

C57BL/6 mice were assigned to a control (20% protein, n = 6), a low protein (4% protein, n = 7), or diets selectively deficient in leucine, arginine, and other essential amino acids (n = 5-6). Colitis was induced by administering 2.5% dextran sulfate sodium in drinking water for 6 d. Intestinal epithelial mTORC1 activity was assessed by immunoblotting. Gut microbiota composition was characterized using 16S sequencing, and the microbiota's role in colitis was evaluated through broad-spectrum antibiotic treatment. Disease severity was quantified by monitoring weight loss, colon shortening, histopathological damage, and inflammatory cytokine expression.

Protein restriction increased the severity of dextran sulfate sodium-induced colitis compared to the control diet (∗∗∗P < 0.001). Mice fed arginine-restricted diets exhibited increased colitis (∗P < 0.05). Protein restriction induced significant alterations in gut microbiota composition, and antibiotic-mediated microbiota depletion partially ameliorated colitis severity, revealing a microbiota-dependent mechanism underlying disease exacerbation.

Our study demonstrates a complex interplay between dietary protein, epithelial mTORC1 signaling, and gut microbiota in modulating IBD pathogenesis and highlights the potential for targeted dietary strategies, including amino acid supplementation, to improve disease management in patients with IBD.

Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disorder of the gastrointestinal tract with limited treatment options. This study investigates the preventive effects of fermented Kamut wheat enzyme (FKW) diet on the progression of dextran sulfate sodium (DSS)-induced colitis in mice, with a focus on gut microbiota modulation and inflammatory cytokine regulation. Female C57BL/6J mice were divided into groups and fed a diet consisting of either a FKW diet (containing 39.80% FKW) or a control diet under 1.25% and 2.50% DSS conditions. The FKW diet was formulated based on the AIN-93G standard rodent formula, with the FKW diet providing comparable amounts of total proteins, crude lipids, and dietary fibers as the control diet. The FKW diet effectively mitigated the progression of colitis, as evidenced by improvements in key indicators such as dietary intake, body weight, colon length, stool consistency, and bleeding, particularly in the 1.25% DSS group. Histopathological analysis revealed preservation of colonic architecture and reduced mucosal damage in the FKW group. The diet also resulted in a significant reduction in pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, and IFN-γ) and myeloperoxidase (MPO) levels, coupled with an increase in anti-inflammatory IL-10. Gut microbiota analysis showed increased abundance of beneficial bacteria such as Muribaculaceae, Lachnospiraceae NK4A136 and Bacteroides acidifaciens and decreased pathogenic bacteria like Escherichia/Shigella and Bilophila. These findings underscore the potential of FKW as a preventive dietary intervention for mitigating the progression of colitis, emphasizing the role of gut microbiota in supporting intestinal health. These results highlight FKW's potential to reduce the risk of colitis development, providing a foundation for future research into its preventive applications.

This comprehensive review examines the impact of dietary patterns on gut microbiome composition and diversity from infancy to old age, linking these changes to age-related health outcomes. It investigates how the gut microbiome develops and changes across life stages, focusing on the influence of dietary factors. The review explores how early-life feeding practices, including breastfeeding and formula feeding, shape the infant gut microbiota and have lasting effects. In elderly individuals, alterations in the gut microbiome are associated with increased susceptibility to infections, chronic inflammation, metabolic disorders and cognitive decline. The critical role of diet in modulating the gut microbiome throughout life is emphasised, particularly the potential benefits of probiotics and fortified foods in promoting healthy ageing. By elucidating the mechanisms connecting food systems to gut health, this review provides insights into interventions that could enhance gut microbiome resilience and improve health outcomes across the lifespan.

Psoriatic arthritis (PsA) is a chronic and progressive inflammatory arthritis associated with psoriasis, mainly affecting the axial and peripheral joints, characterized by a wide range of complex phenotypes, significant heterogeneity, and a multifactorial etiology. To effectively address the distinct challenges in managing PsA, a pivotal emphasis is placed on clarifying the concept of refractory PsA. Here, we propose a distinction between refractory PsA, differentiating between difficult-to-treat PsA (D2T PsA) and Pseudo-D2T PsA. The former centers on the lack of efficacy of multiple disease-modifying anti-rheumatic drugs (DMARDs) and signs suggestive of active/progressive disease, while also considering the challenges posed by comorbidities. The latter focuses on misdiagnosis and mismanagement, detailing the difficulties caused by artificial factors, whether by clinicians or patients. Hoping the clarification of these distinctions will enable clinicians to manage patients with refractory PsA more effectively.

Plant-derived extracellular vesicles (PDEVs) are membrane vesicles characterized by a phospholipid bilayer as the basic skeleton that is wrapped by various functional components of proteins and nucleic acids. An increasing number of studies have confirmed that PDEVs can be a potential treatment of inflammatory bowel disease (IBD) and can, to some extent, compensate for the limitations of existing therapies.

This review summarizes the recent advances and potential mechanisms underlying PDEVs obtained from different sources to alleviate IBD. In addition, the review discusses the possible applications and challenges of PDEVs, providing a theoretical basis for exploring novel and practical therapeutic strategies for IBD.

In IBD, the crosstalk mechanism of PDEVs may regulate the intestinal microenvironment homeostasis, especially immune responses, the intestinal barrier, and the gut microbiota. In addition, drug loading enhances the therapeutic potential of PDEVs, particularly regarding improved tissue targeting and stability. In the future, not only immunotherapy based on PDEVs may be an effective treatment for IBD, but also the intestinal barrier and intestinal microbiota will be a new direction for the treatment of IBD.

Whether improvements in gastrointestinal (GI) symptoms observed with Elexacaftor/Tezacaftor/Ivacaftor (ETI) treatment are sustained in the longer-term requires exploration. This study investigated how GI-symptoms change with longer-term ETI use in pancreatic insufficient adults with cystic fibrosis (awCF).

Participants completed up to three abdominal symptom questionnaires, employing the validated CFAbd-Score. Changes in total CFAbd-Score and its five domains, pain, gastroesophageal reflux-disease (GERD), disorders of bowel movement (DBM), disorders of appetite (DA) and quality of life (QOL), were analysed pre-ETI (T0) and at ≤1.5 years (T1) and 2-4 years of ETI-therapy (T2).

A total of 165 CFAbd-Scores from 68 participants were analysed (median age: 34 years; IQR: 28-39). Total CFAbd-Score significantly (p < 0.05) and clinically meaningfully decreased from 20.4 ± 1.6 pre-ETI (median:40 weeks pre-treatment) to 15.3 ± 1.9 and 16.8 ± 1.6 at T1 (median: 25 weeks of ETI) and T2 (median: 148 weeks of ETI), respectively. The CFAbd-Score´s domains DA and QoL only significantly decreased between T0 and T1, whereas DBM only significantly decreased after 2-4 years of ETI therapy (T2). GERD scores were significantly lower at both T1 and T2.

While GI symptoms in awCF significantly improve within the first 1.5 years of ETI-therapy, they appear to somewhat wane with longer-term use, despite GI-symptom burden still being lower compared to pre-ETI. However, we cannot differentiate whether this results from reduced adherence, a decrease in ETI effects, or long-term changes in diet, gut microbiota or symptom perception. The longer-term impact of ETI and other potential modulator therapies on GI symptoms requires ongoing monitoring.

Inflammatory Bowel Disease (IBD) is increasing worldwide and has become a global emergent disease. Probiotics have been reported to be effective in relieving colitis. Previous studies found ripened Pu-erh tea (RPT) promoted gut microbiota resilience against dextran sulfate sodium (DSS)-induced colitis in mice by increasing relative abundance of Lactobacillus. However, whether and how it alleviated DSS-induced colitis in mice need to be explored. Here, we screened a probiotic Lactobacillus johnsonii GLJ001 from feces of ripened Pu-erh tea (RPT)-administrated mice. In this study, L. johnsonii GLJ001 attenuated symptoms of DSS-induced colitis in mice, including weight loss, increased disease activity index (DAI), colon shortening and colon tissue damage, as well as high expression of inflammatory cytokines and disturbances of intestine barrier function. Furthermore, abundances of short-chain fatty acids (SCFAs)-producing bacteria (i.e. Clostridium cluster IV and XIVa, Lachnospiracea_incertae_sedis and Ruminococcus) were enhanced in the cecum of mice treated with L. johnsonii GLJ001, accompanying by an increase of SCFAs. It was also found that SCFAs inhibited mRNA expression of M1 macrophage markers (Inos and CD86), inflammatory cytokines (TNF-α and Il-1β) and SCFAs receptors (Gpr41 and Gpr43) induced by lipopolysaccharide (LPS) and interferon-γ (IFN-γ) in THP-1 cell line. Collectively, L. johnsonii GLJ001 prevented DSS-induced colitis in mice by inhibiting M1 macrophage polarization via gut microbiota-SCFAs axis, and can be administered for management of colitis.

The relationship between gut microbiota composition, lifestyles, and colonic transit time (CTT) remains poorly understood. This study investigated associations among gut microbiota profiles, diet, lifestyles, and CTT in individuals with subjective constipation.

We conducted a secondary analysis of data from our randomized clinical trial, examining gut microbiota composition, CTT, and dietary intake in baseline and final assessments of 94 participants with subjective constipation. Participants were categorized into normal-transit (<36 h) and slow-transit (≥36 h) groups based on CTT at baseline. Gut microbiota composition was measured using 16S rRNA sequencing, and dietary patterns were assessed through semi-quantitative food frequency questionnaires. Enterotype analysis, machine learning approaches, and metabolic modeling were employed to investigate microbiota-diet interactions. The constipated participants primarily belonged to Lachnospiraceae (ET-L).

The slow-transit group showed higher alpha diversity than the normal-transit group. Butyricicoccus faecihominis was abundant in the normal-transit group, while Neglectibacter timonensis, Intestinimonas massiliensis, and Intestinibacter bartlettii were abundant in the slow-transit group, which also had a higher abundance of mucin-degrading bacteria. Metabolic modeling predicted increased N-acetyl-D-glucosamine (GlcNAc), a mucin-derived metabolite, in the slow-transit group. Network analysis identified two microbial co-abundance groups (CAG3 and CAG9) significantly associated with transit time and dietary patterns. Six mucin-degrading species showed differential correlations with GlcNAc and a plant-based diet, particularly, including rice, bread, fruits and vegetables, and fermented beans. In conclusion, an increased abundance of mucin-degrading bacteria and their predicted metabolic products were associated with delayed CTT.

These findings suggest dietary modulation of these bacterial populations as a potential therapeutic strategy for constipation. Moreover, our results reveal a potential immunometabolic mechanism where mucin-degrading bacteria and their metabolic interactions may influence intestinal transit, mucosal barrier function, and immune response.

Background/Objectives: Dietary patterns, including high-fat and high-carbohydrate diets (HFDs and HCDs), as well as non-dietary factors such as food additives and antibiotics, are strongly linked to metabolic endotoxemia, a critical driver of low-grade chronic inflammation. This review explores the mechanisms through which these factors impair intestinal permeability, disrupt gut microbial balance, and facilitate lipopolysaccharide (LPS) translocation into the bloodstream, contributing to metabolic disorders such as obesity, type 2 diabetes mellitus, and inflammatory bowel disease. Methods: The analysis integrates findings from recent studies on the effects of dietary components and gut microbiota interactions on intestinal barrier function and systemic inflammation. Focus is given to experimental designs assessing gut permeability using biochemical and histological methods, alongside microbiota profiling in both human and animal models. Results: HFDs and HCDs were shown to increase intestinal permeability and systemic LPS levels, inducing gut dysbiosis and compromising barrier integrity. The resulting endotoxemia promoted a state of chronic inflammation, disrupting metabolic regulation and contributing to the pathogenesis of various metabolic diseases. Food additives and antibiotics further exacerbated these effects by altering microbial composition and increasing gut permeability. Conclusions: Diet-induced alterations in gut microbiota and barrier dysfunction emerge as key mediators of metabolic endotoxemia and related disorders. Addressing dietary patterns and their impact on gut health is crucial for developing targeted interventions. Further research is warranted to standardize methodologies and elucidate mechanisms for translating these findings into clinical applications.

The gut microbiota plays a vital role in various physical and physiological processes, including immune system regulation, neurotransmitter production, inflammatory response modulation, and the inhibition of pathogenic organisms. An imbalance in the microbial community, known as dysbiosis, has been associated with numerous health issues. Biological influences, health behaviors, socioeconomic determinants, and nutritional status can disrupt this balance.

To evaluate the differences in the gut microbiota composition in medical students according to fiber intake, ultra-processed food (UPF) consumption, sex, body mass index, and socioeconomic status.

A cross-sectional study was conducted with 91 medical students, and 82 fecal samples were analyzed. Sociodemographic and dietary data were collected via questionnaires, UPF consumption was assessed using the NOVA classification, and trained nutritionists performed anthropometry. DNA extraction and 16S rRNA sequencing were performed for the microbial analysis. Bioinformatics and statistical tests included the Dunn and Kruskal-Wallis tests, a PCoA analysis, PERMANOVA, ANOVA, Spearman's rank correlation, and alpha and beta diversity metrics.

Dietary fiber intake strongly influences gut microbiota composition. Lower fiber intake was associated with a higher prevalence of Parabacteroides and Muribaculaceae. Prevotella was more prevalent in individuals with lower UPF intake, while Phascolarctobacterium was prevalent in those with higher UPF consumption. Significant differences were associated with sex and UPF consumption but not BMI or SES. Women consumed more UPF, which correlated with distinct gut microbiota profiles.

This study highlights the significant impact of diet, particularly fiber intake and UPF, on gut microbiota composition, emphasizing the importance of dietary habits in maintaining gut health.

Imbalances in Th1/Th2 and Th17/Treg immune axes, coupled with disruptions in the gut microbiota (GM), play a pivotal role in the pathogenesis of inflammatory bowel disease (IBD). Cordycepin, a natural anti-inflammatory compound, holds promise in mitigating IBD by rebalancing these immune axes in conjunction with modulating the GM. The aim of this experiment is to investigate the potential of cordycepin in mitigating enteritis and elucidate the underlying mechanisms associated with its ameliorative effects on enteritis.

On the day of inducing experimental colitis with Dextran Sulfate Sodium (DSS), mice in the DSS + Cordycepin and Cordycepin groups received 50 mg/kg/day Cordycepin via intra-gastric administration (i.g.) for seven consecutive days, respectively. Mice in the DSS and control groups were treated with equal volumes of saline. On day 8, all mice were euthanized under pentobarbital sodium anesthesia.

In a DSS-induced colitis mouse model, Cordycepin treatment led to a significant reduction in the disease activity index (DAI), splenic weight, and colonic pathological injury while simultaneously improving body weight and colonic length. Furthermore, it positively impacted GM composition, resulting in decreased Th1 and Th17 cells, alongside an increase in Th2 and Treg cells. The contents of the mouse colon were extracted for microbial community analysis. Mouse blood was prepared into a single-cell suspension, and flow cytometry was used to assess the expressio of Treg, Th17, Th1, and Th2 immune cells.

These results underscored the effective intervention of cordycepin in ameliorating DSS-induced colitis by harmonizing the interplay between GM and immune homeostasis.

As a classical traditional Chinese medicine formula to invigorating spleen and replenishing qi, Sijunzi decoction (SJZD) is composed of four herbs, which is applied to cure spleen deficiency syndrome (SDS) clinically. The non-polysaccharides (NPSs) of SJZD (SJZD_NPS) are important pharmacodynamic material basis. However, the amelioration mechanism of SJZD_NPS on SDS has not been fully elaborated. Additionally, the contribution of herbs compatibility to efficacy of this formula remains unclear.

The aim was to explore the underlying mechanisms of SJZD_NPS on improving SDS, and uncover the scientific connotation in SJZD compatibility.

A strategy integrating incomplete formulae (called "Chai-fang" in Chinese) comparison, pharmacodynamics, gut microbiome, and metabolome was employed to reveal the role of each herb to SJZD compatibility against SDS. Additionally, the underlying mechanism harbored by SJZD_NPS was further explored through targeted metabolomics, network pharmacology, molecular docking, pseudo-sterile model, and metagenomics.

SJZD_NPS significantly alleviated diarrhea, disordered secretion of gastrointestinal hormones and neurotransmitters, damage of ileal morphology and intestinal barrier in SDS rats, which was superior to the NPSs of Chai-fang. 16S rRNA gene sequencing and metabolomics analyses revealed that SJZD_NPS effectively restored the disturbed gut microbiota community and abnormal metabolism caused by SDS, showing the most evident recovery. Moreover, SJZD_NPS recalled the levels of partial amino acids, short chain fatty acids and bile acids, which possessed strong binding affinity towards potential targets. The depletion of gut microbiota confirmed that the SDS-amelioration efficacy of SJZD_NPS is dependent on the intact gut microbiome, with the relative abundance of potential probiotics such as Lactobacillus_johnsonii and Lactobacillus_taiwanensis been enriched.

NPSs in SJZD can improve SDS-induced gastrointestinal-nervous system dysfunction through regulating microbiota-gut-metabolites axis, with four herbs exerting synergistic effects, which indicated the compatibility rationality of SJZD.

The role of the environment in the pathogenesis of inflammatory bowel disease (IBD) is undisputed, especially in light of numerous epidemiological data showing the increasing prevalence of IBD worldwide. Although no specific environmental factors have been identified, the diet has received the most attention as a potential modifier of the onset and course of IBD and as a therapeutic intervention. The Westernization of the diet is repeatedly cited as a crucial aspect of the change in IBD prevalence, but data on the impact of diet on the course of IBD are still limited and the effectiveness of dietary interventions remains uncertain. Milk remains one of the most discussed dietary agents in IBD.

We performed a systematic review of the literature published between January 2010 and March 2024 on three databases, Pubmed, Web of Knowledge, and Embase, to assess the impact of milk and dairy products on the risk and course of IBD, as well as patients' dietary beliefs and practices.

We included 37 original studies in our review.

There is no clear evidence that milk and dairy products influence the incidence and course of IBD. The studies that assess this issue are characterized by great heterogeneity. Milk and dairy are among the most commonly excluded foods by patients with IBD, which may have clinical implications.

Crohn's disease (CD) is a sub-type of inflammatory bowel disease (IBD) with a characteristic relapsing and remitting inflammation involving the gastrointestinal (GI) tract. Although there are several medications to relieve the symptoms, there is no definite cure for the condition. This paper highlights how CD affects our gut flora, which subsequently leads to the perpetuation of inflammation. This review was conducted according to Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) 2020 guidelines using PubMed, ScienceDirect, Multidisciplinary Digital Publishing Institute (MDPI), and Google Scholar as sources for relevant literature. After applying the quality appraisal tools, we finalized 11 articles for the paper. Inflammation seen in CD leads to dysbiosis, where there is a reduction in beneficial microbes such as Faecalibacterium and Roseburia species and an increase in pathogenic microbes such as Escherichia and Proteus species. This difference in gut microbes disrupts barrier function and immune processes in the intestine, contributing to the worsening of inflammation seen in CD. Several studies have been carried out to understand this complex relationship between the gut microbiome (GM) and CD, as it may serve as a potential novel therapeutic alternative, necessary as CD's burden is increasing globally.

The increasing prevalence of noncommunicable diseases in the aging population has been correlated with a decline in innate and adaptive immune responses; hence, it is imperative to identify approaches to improve immune function, prevent related disorders, and reduce or treat age-associated health complications. Prebiotic supplementation is a promising approach to modulate the gut microbiome and immune system, offering a potential strategy to maintain the integrity of immune function in older individuals. This review summarizes the current research on prebiotic galacto-oligosaccharide (GOS) immunomodulatory mechanisms mediated by bacterial-derived metabolites, including short-chain fatty acids and secondary bile acids, to maintain immune homeostasis. The potential applications of GOS as immunotherapy for age-related disease prevention in older individuals are also highlighted. This aligns with the global shift toward proactive healthcare and emphasizes the significance of early intervention in directing an individual's health trajectory.

The escalation of urbanization correlates with rising rates of inflammatory bowel disease (IBD), necessitating research into new etiological factors. This study aims to elucidate the gut microbiota profiles in IBD patients and compare them with healthy controls in a western city of China.

We conducted a multicenter case-control study from the end of 2020, using 16S rRNA gene sequencing (n = 36) and metagenomic sequencing (n = 12) to analyze the gut microbiota of newly diagnosed IBD patients, including those with Crohn's disease (CD) and ulcerative colitis (UC).

Our results demonstrated a significant enrichment of the phylum Proteobacteria, particularly the genus Escherichia-Shigella, in CD patients. Conversely, the genus Enterococcus was markedly increased in UC patients. The core gut microbiota, such as the Christensenellaceae R-7 group, Fusicatenibacter, and Holdemanella, were primarily identified in healthy subjects. Additionally, significant interactions between the microbiome and virulence factors were observed.

The findings suggest that oxidative stress may play a pivotal role in the pathology of IBD. This study contributes to the growing dialogue about the impact of gut microbiota on the development of IBD and its variations across different geographies, highlighting potential avenues for further research.

Inflammatory bowel disease (IBD), mainly comprising ulcerative colitis and Crohn's disease, is a group of gradually progressive diseases bringing significant mental anguish and imposes serious economic burdens. Interplay of genetic, environmental, and immunological factors have been implicated in its pathogenesis. Nutrients, as crucial environmental determinants, mainly encompassing carbohydrates, fats, proteins, and micronutrients, are closely related to the pathogenesis and development of IBD. Nutrition is essential for maintaining the dynamic balance of intestinal eco-environments to ensure intestinal barrier and immune homeostasis, while this balance can be disrupted easily by maladjusted nutrition. Research has firmly established that nutrition has the potential to shape the composition and function of gut microbiota to affect the disease course. Unhealthy diet and eating disorders lead to gut microbiota dysbiosis and further destroy the function of intestinal barrier such as the disruption of membrane integrity and increased permeability, thereby triggering intestinal inflammation. Notably, appropriate nutritional interventions, such as the Mediterranean diet, can positively modulate intestinal microecology, which may provide a promising strategy for future IBD prevention. In this review, we provide insights into the interplay between nutrition and gut microbiota and its effects on IBD and present some previously overlooked lines of evidence regarding the role of derived metabolites in IBD processes, such as trimethylamine N-oxide and imidazole propionate. Furthermore, we provide some insights into reducing the risk of onset and exacerbation of IBD by modifying nutrition and discuss several outstanding challenges and opportunities for future study.

Previous observational studies have suggested an association between tryptophan (TRP)-kynurenine (KYN) pathway and inflammatory bowel disease (IBD). However, whether there is a causal relationship among them remains unclear. Therefore, a two-sample Mendelian randomization (MR) study was conducted to explore the potential causal effects of crucial metabolites in TRP-KYN pathway on IBD and its subtypes. Using summary data from genome-wide association studies, a two-sample MR was employed to evaluate the genetic associations between TRP and KYN as exposures and IBD as an outcome. The inverse variance weighted method was used as the primary MR analysis, with MR-Egger, weighted mode, simple mode, and weighted median methods as complementary analyses. The odds ratios (OR) and 95% confidence intervals (CI) were determined for TRP-IBD (OR 0.739, 95% CI [0.697; 0.783]), TRP-UC (OR 0.875, 95% CI [0.814; 0.942]), TRP-CD (OR 0.685, 95% CI [0.613; 0.765]), KYN-IBD (OR 4.406, 95% CI [2.247; 8.641]), KYN-UC (OR 2.578, 95% CI [1.368; 4.858], and KYN-CD (OR 13.516, 95% CI [4.919; 37.134]). Collectively, the MR analysis demonstrated a significant protective association between TRP and IBD, whereas KYN was identified as a risk factor for IBD.

Inflammatory bowel disease (IBD) is a chronic and recurrent condition affecting the gastrointestinal tract. Disturbed gut microbiota and abnormal bile acid (BA) metabolism are notable in IBD, suggesting a bidirectional relationship. Specifically, the diversity of the gut microbiota influences BA composition, whereas altered BA profiles can disrupt the microbiota. IBD patients often exhibit increased primary bile acid and reduced secondary bile acid concentrations due to a diminished bacteria population essential for BA metabolism. This imbalance activates BA receptors, undermining intestinal integrity and immune function. Consequently, targeting the microbiota-BA axis may rectify these disturbances, offering symptomatic relief in IBD. Here, the interplay between gut microbiota and bile acids (BAs) is reviewed, with a particular focus on the role of gut microbiota in mediating bile acid biotransformation, and contributions of the gut microbiota-BA axis to IBD pathology to unveil potential novel therapeutic avenues for IBD.

Inflammatory bowel disease (IBD) is a chronic and idiopathic condition that results in inflammation of the gastrointestinal tract, leading to conditions such as ulcerative colitis and Crohn's disease. Commonly used treatments for IBD include anti-inflammatory drugs, immunosuppressants, and antibiotics. Fecal microbiota transplantation is also being explored as a potential treatment method; however, these drugs may lead to systemic side effects. Oral administration is preferred for IBD treatment, but accurately locating the inflamed area in the colon is challenging due to multiple physiological barriers. Nanoparticle drug delivery systems possess unique physicochemical properties that enable precise delivery to the target site for IBD treatment, exploiting the increased permeability and retention effect of inflamed intestines. The first part of this review comprehensively introduces the pathophysiological environment of IBD, covering the gastrointestinal pH, various enzymes in the pathway, transport time, intestinal mucus, intestinal epithelium, intestinal immune cells, and intestinal microbiota. The second part focuses on the latest advances in the mechanism and strategies of targeted delivery using oral nanoparticle drug delivery systems for colitis-related fields. Finally, we present challenges and potential directions for future IBD treatment with the assistance of nanotechnology.

As the global population ages, the prevalence of neurodegenerative diseases is surging. These disorders have a multifaceted pathogenesis, entwined with genetic and environmental factors. Emerging research underscores the profound influence of diet on the development and progression of health conditions. Intermittent fasting (IF), a dietary pattern that is increasingly embraced and recommended, has demonstrated potential in improving neurophysiological functions and mitigating pathological injuries with few adverse effects. Although the precise mechanisms of IF's beneficial impact are not yet completely understood, gut microbiota and their metabolites are believed to be pivotal in mediating these effects. This review endeavors to thoroughly examine current studies on the shifts in gut microbiota and metabolite profiles prompted by IF, and their possible consequences for neural health. It also highlights the significance of dietary strategies as a clinical consideration for those with neurological conditions.

In this study, we investigated the effects of Lactobacillus johnsonii on the mouse colitis model. The results showed that the supernatant of the L. johnsonii culture alleviated colitis and remodeled gut microbiota, represented by an increased abundance of bacteria producing short-chain fatty acids, leading to an increased concentration of propionic acid in the intestine. Further studies revealed that propionic acid inhibited activation of the MAPK signaling pathway and polarization of M1 macrophages. Macrophage clearance assays confirmed that macrophages are indispensable for alleviating colitis through propionic acid. In vitro experiments showed that propionic acid directly inhibited the MAPK signaling pathway in macrophages and reduced M1 macrophage polarization, thereby inhibiting the secretion of pro-inflammatory cytokines. These findings improve our understanding of how L. johnsonii attenuates inflammatory bowel disease (IBD) and provide valuable insights for identifying molecular targets for IBD treatment in the future.

The anti-inflammatory effect of ellagic acid (EA) and its possible underlying mechanism in dextran sulfate sodium (DSS)-induced mouse chronic colonic inflammation were studied. It was observed that EA administration significantly alleviated the colonic inflammation phenotypes, including decreasing the disease activity index (DAI), enhancing the body weight loss, and improving the shortened length of the colon and pathological damage of colon tissue. Additionally, EA reshaped the constitution of the gut microbiota by elevating the ratio of Bacteroidetes along with Bacteroides and Muribaculaceae, while decreasing the proportion of Firmicutes. The Phylogenetic Investigation of Communities by Reconstruction of Unobserved States 2 (PICRUSt2) revealed that the metabolic function of the gut microbiota was also changed. Furthermore, mouse colon transcriptome analysis showed that the tight junction and peroxisome proliferator-activated receptor (PPAR) signaling pathways were activated and the expressions of related genes were upregulated after EA intervention. These results showed that EA could remodel the gut bacterial composition, change the intestinal epithelial cell gene expressions in mice, and consequently improve the colonic inflammatory symptoms.

The epidemic of coronavirus disease-19 (COVID-19) has grown to be a global health threat. Gastrointestinal symptoms are thought to be common clinical manifestations apart from a series of originally found respiratory symptoms. The human gut harbors trillions of microorganisms that are indispensable for complex physiological processes and homeostasis. Growing evidence demonstrate that gut microbiota alteration is associated with COVID-19 progress and severity, and post-COVID-19 syndrome, characterized by decrease of anti-inflammatory bacteria like Bifidobacterium and Faecalibacterium and enrichment of inflammation-associated microbiota including Streptococcus and Actinomyces. Therapeutic strategies such as diet, probiotics/prebiotics, herb, and fecal microbiota transplantation have shown positive effects on relieving clinical symptoms. In this article, we provide and summarize the recent evidence about the gut microbiota and their metabolites alterations during and after COVID-19 infection and focus on potential therapeutic strategies targeting gut microbiota. Understanding the connections between intestinal microbiota and COVID-19 would provide new insights into COVID-19 management in the future.

Gut dysbiosis and bile acid (BA) metabolism disturbance are involved in the pathogenesis of ulcerative colitis. This study aimed to investigate the effect of fucoidan on BA metabolism and gut microbiota in dextran sulfate sodium-induced colitis mice. Our results showed that fucoidan effectively suppressed colonic inflammation and repaired the gut barrier. In addition, fucoidan increased the relative abundance of the Lachnospiraceae family, such as Turicibacter, Muribaculum, Parasutterella, and Colidextribacter, followed by an increase in short-chain fatty acids, especially in butyrate. Moreover, fucoidan modulated bile acid metabolism by elevating cholic acid, ursodeoxycholic acid, deoxycholic acid, and lithocholic acid and decreasing β-muricholic acid, which led to activation of FXR and TGR5 and further enhanced the gut barrier and suppressed colonic inflammation. Our results revealed that the effect of fucoidan alleviating colitis was largely mediated by gut microbiota, which was confirmed by the fecal transplantation experiment. Collectively, these findings provided the basis for fucoidan as a potential functional food for colitis.