Type 2 diabetes mellitus (T2DM) is a complex metabolic disorder characterized by hyperglycemia and insulin resistance. Plantain shell powder (PHP) serves as a high-quality source of dietary fiber, widely utilized in food additives and pharmaceutical applications. In this study, we investigated the hypoglycemic activity and underlying mechanisms of PHP by examining its effects on intestinal microbiota and metabolism in T2DM mice induced by a high-fat diet and streptozotocin (STZ). Our findings indicate that PHP significantly enhances blood glucose homeostasis and insulin sensitivity, reduces organ damage, and regulates blood lipid levels as well as short-chain fatty acid concentrations; notably, higher doses of PHP yielded optimal results. In addition, PHP can regulate the ratio of Bacteroidota to Firmicutes and increase the relative abundance of beneficial bacteria such as Bacteroidales, Muribaculaceae, and Parabacteroides. Furthermore, PHP enhances the enrichment of key metabolic pathways, including α-linolenic acid metabolism, monobactam biosynthesis, and PPAR signaling pathways, thereby promoting the production of beneficial metabolites. Complex interactions exist among these beneficial bacteria and metabolic pathways that are associated with improved metabolic function, regulation of glucose homeostasis, enhancement of insulin sensitivity, and reduction of inflammation. Our study demonstrates that PHP can ameliorate T2DM by reversing alterations in gut microbiota and metabolic profiles caused by T2DM while promoting the regulation of beneficial microbial populations.

The gut microbiome is recognized as a critical factor in advancing precision nutrition and medicine for health and in developing dietary recommendations and targeted therapies for gastrointestinal (GI) health and diseases. However, conventional sampling methods, such as fecal analysis and colonoscopy, often fail to capture microbial information from specific regions of the GI tract or require invasive procedures, thereby limiting accuracy and clinical utility. As a non-invasive alternative, passive sampling capsules have been developed for site-specific microbiome analysis by employing pH-sensitive enteric coatings that delay sampling until the capsule reaches the targeted intestinal region. Although this approach has been successful in the small intestine, colonic sampling remains challenging due to the high interpersonal variability in intestinal pH, which makes it difficult to rely solely on a pH-triggering mechanism. To overcome this challenge, a dual bacterially and pH triggered polymeric enteric coating was created by blending lactulose and N,N-dimethylaminoethyl methacrylate, enabling complete dissolution within the colonic region. Through systematic characterization of multiple polymer blend compositions using Fourier Transform Infrared Spectroscopy, Thermogravimetric Analysis, and Differential Scanning Calorimetry, an optimized design was identified that provides both suitable physical integrity and rapid (∼2 h) degradation in the presence of colonic bacteria, across a pH range of 5 to 8. The optimized blend was subsequently applied as a double-layer enteric coating on a sampling capsule, enabling the dissolution of the outer layer in the small intestine and complete dissolution of the inner layer in the colon. In-vitro and in-vivo pig model studies were conducted to validate the capsule's sampling performance and to ensure the preservation of the microbial environment. Furthermore, 16S rRNA sequencing revealed a taxonomic similarity between samples collected by the capsule and the colonic microbiome (residing between the ileum and fecal matter). Overall, this technology provides an effective approach to targeted microbial sampling and may pave the way for more comprehensive colonic microbiome analyses and improved diagnostic capabilities for GI diseases. STATEMENT OF SIGNIFICANCE: Precise monitoring of the gut microbiome is vital for understanding health and disease, yet current sampling techniques often lack precision or require invasive procedures. Our work introduces a novel, non-invasive capsule that targets the colon using a dual-trigger polymer system activated by both pH and colonic bacteria. This design enables localized sampling of gut microbiota, overcoming the limitations of fecal analysis, endoscopy, and earlier pH-triggered capsule designs. By capturing microbial communities directly from the colon, our technology provides deeper insights into colonic health and conditions such as inflammatory bowel disease and colorectal cancer. This breakthrough represents a significant advancement in precision nutrition and medicine for human health, and advanced diagnostics and targeted therapies to support dietary guidance, clinical practice and biomedical research.

Bacteriophages (phages) play a crucial role in shaping the composition and diversity of the human microbiome across various body niches. Recent advancements in high-throughput sequencing technologies have enabled comprehensive analysis of the human phageome in different body sites. This review comprehensively analyzes phage populations across major human body niches, examining their distribution and dynamics through recent metagenomic discoveries. We explore how phage-bacteria interactions within different body sites contribute to homeostasis and disease development. Emerging evidence demonstrates that phageome perturbations can serve as early indicators of various disorders, particularly in the gut microbiome. Understanding these complex microbial interactions offers promising opportunities for developing novel diagnostic markers and therapeutic approaches. However, the causal relationship between phages, bacteria, and disease development remains unclear. Further research is needed to elucidate the role of phages in human health and disease and to explore their potential as diagnostic or therapeutic tools. Understanding the intricate interactions between phages, bacteria, and the human host is crucial for unraveling the complexities of the human microbiome and its impact on health and disease.

Previous observational studies have indicated a correlation between the skin microbiome and Type 2 diabetes (T2DM). It is hypothesized that this causal relationship may be influenced by inflammatory responses. However, these factors as determinants of T2DM remain largely unexplored.

This study incorporated data from the GWAS database on the skin microbiome, 91 types of inflammatory cytokines, and T2DM. We employed two-sample MR and multivariable MR methods to assess the correlation between the skin microbiome and T2DM, and to investigate whether this correlation is affected by inflammatory cytokines.

The results of the two-sample MR analysis indicate that within the skin microbiome, genetically predicted genus: Acinetobacter, class: Alphaproteobacteria, genus: Bacteroides, ASV005[Propionibacterium granulosum], and ASV072[Rothia mucilaginosa] are associated with an increased risk of T2DM, while phylum: Proteobacteria, genus: Enhydrobacter, family: Clostridiales, ASV006[Staphylococcus hominis] serve as protective factors against T2DM. Among the inflammatory cytokines, levels of Macrophage colony-stimulating factor 1, Tumor necrosis factor receptor superfamily member 9, Urokinase-type plasminogen activator, and C-C motif chemokine 28 are associated with an increased risk of T2DM. Multivariable MR analysis further revealed that Macrophage colony-stimulating factor 1 levels act as a mediating factor between ASV072[Rothia mucilaginosa] and T2DM.

In this study, we found a connection between the skin microbiome and T2DM, with inflammatory cytokines playing a key role in this relationship. This research helps us better understand this complex link and shows that addressing inflammation is important for preventing and treating diabetes. This could greatly benefit public health by reducing the impact of diabetes and its complications. Our results suggest that future studies should explore the specific biological interactions between the skin microbiome and diabetes to develop more effective risk management and treatment strategies from a microbial perspective.

Tuberculosis, primarily caused by Mycobacterium tuberculosis, is an airborne lung disease and continues to pose a significant global health threat, resulting in millions of deaths annually. The current treatment for tuberculosis involves a prolonged regimen of antibiotics, which leads to complications such as recurrence, drug resistance, reinfection, and a range of side effects. This scenario underscores the urgent need for novel therapeutic strategies to combat this lethal pathogen. Over the last two decades, microbiome therapeutics have emerged as promising next-generation drug candidates, offering advantages over traditional medications. In 2022, the Food and Drug Administration approved the first microbiome therapeutic for recurrent Clostridium infections, and extensive research is underway on microbiome treatments for various challenging diseases, including metabolic disorders and cancer. Research on microbiomes concerning tuberculosis commenced roughly a decade ago, and the scope of this research has broadened considerably over the last five years, with microbiome therapeutics now viewed as viable options for managing drug-resistant tuberculosis. Nevertheless, the understanding of their mechanisms is still in its infancy. Although autophagy has been extensively studied in other diseases, research into its role in tuberculosis is just beginning, with preliminary developments in progress. Against this backdrop, this comprehensive review begins by succinctly outlining tuberculosis' characteristics and assessing existing treatments' strengths and weaknesses, followed by a detailed examination of microbiome-based therapeutic approaches for drug-resistant tuberculosis. Additionally, this review focuses on establishing a basic understanding of microbiome treatments for tuberculosis, mainly through the lens of autophagy as a mechanism of action. Ultimately, this review aims to contribute to the foundational comprehension of microbiome-based therapies for tuberculosis, thereby setting the stage for the further advancement of microbiome therapeutics for drug-resistant tuberculosis.

To date, bariatric surgery (BS) is the most effective long-term treatment for obesity, but weight regain (WR) is common. The very low-calorie ketogenic diet (VLCKD) is effective for weight loss and may influence gut microbiota (GM) composition, but it has been scarcely evaluated in post-bariatric patients. This study compared the efficacy and safety of a VLCKD in patients with WR post-bariatric surgery (BS+) and in bariatric surgery-naïve patients (BS-).

In this prospective, case-control study, 33 patients (15 BS+, 18 BS-) underwent an 8-week-long VLCKD. Outcomes included weight loss, metabolic profile, safety and GM composition.

Both groups achieved significant weight loss (BS+: -6.9%, BS-: -8.3%), but the BS+ group showed slightly less metabolic improvement, particularly in insulin resistance and triglycerides. GM composition differed at baseline, reflecting the lasting effects of BS, and VLCKD led to significant changes in both groups. Microbial diversity and specific taxonomic shifts were more pronounced in BS- patients. Mild renal function changes were noted in BS+ patients, though these remained within clinically acceptable ranges.

VLCKD is effective in both BS+ and BS- patients, though metabolic and microbial responses may be less robust post-surgery, possibly due to anatomical and physiological changes. Tailored approaches may be therefore needed to optimize outcomes in post-bariatric patients.

The intestinal microbiome constitutes a sophisticated and massive ecosystem pivotal for maintaining gastrointestinal equilibrium and mucosal immunity via diverse pathways. The gut microbiota is continuously reshaped by multiple environmental factors, thereby influencing overall wellbeing or predisposing individuals to disease state. Many observations reveal an altered microbiome composition in individuals with autoimmune conditions, coupled with shifts in metabolic profiles, which has spurred ongoing development of therapeutic interventions targeting the microbiome. This review delineates the microbial consortia of the intestine, their role in sustaining gastrointestinal stability, the association between the microbiome and immune-mediated pathologies, and therapeutic modalities focused on microbiome modulation. We emphasize the entire role of the intestinal microbiome in human health and recommend microbiome modulation as a viable strategy for disease prophylaxis and management. However, the application of gut microbiota modification for the treatment of immune-related diseases, such as fecal microbiota transplantation and probiotics, remain quite challenging. Therefore, more research is needed into the role and mechanisms of these therapeutics.

Obesity affects the adaptability of adipose tissue (AT), impairing its ability to regulate energy and metabolism. Obesity is associated with many metabolic disorders, including dyslipidemia, hypertension, sleep disorders, non-alcoholic liver disease, and some types of cancer. Toll-like receptors (TLRs) are important in obesity and related metabolic disorders. TLRs are pattern-recognizing receptors (PRRs) involved in the innate immune system and recognize pathogen-associated molecular patterns (PAMPs) and endogenous ligands. TLRs, especially TLR2 and TLR4, are activated by fatty acids, endotoxins, and other ligands. TLR2 and TLR4 activation triggers inflammatory responses. Chronic inflammation driven by TLR activation is a hallmark of obesity and metabolic diseases. The inflammatory response triggered by TLR activation alters insulin signaling, contributing to insulin resistance, a key feature of metabolic syndrome and type 2 diabetes. Modulation of TLR activity through lifestyle changes (diet and exercise), obesity surgery, and pharmacological agents is under study as a possible therapeutic approach to controlling obesity and its complications.

There are limited longitudinal data from non-industrialized settings on patterns and determinants of gut bacterial microbiota development in early childhood. We analysed epidemiological data and stool samples collected from 60 children followed from early infancy to 5 years of age in a rural tropical district in coastal Ecuador. Data were collected longitudinally on a wide variety of individual, maternal, and household exposures. Extracted DNA from stool samples were analysed for bacterial microbiota using 16S rRNA gene sequencing. Both alpha and beta diversity indices suggested stable profiles towards 5 years of age. Greater alpha diversity and lower beta diversity were associated with factors typical of rural poverty including low household incomes, overcrowding, and greater agricultural and animal exposures. Consumption of unpasteurized milk was consistently associated with greater alpha diversity indices. Delivery method and antibiotic exposures during pregnancy and early childhood appeared to have limited effects on developmental trajectories of gut microbiota. Infants living in a non-industrialized setting in conditions of greater poverty and typically rural exposures appeared to acquire more rapidly a stable and diverse gut bacterial microbiome during childhood.

This study aims to investigate the characteristics of gut microbiota in patients with microvascular complications of Type 2 Diabetes Mellitus (T2DM) using 16S rRNA high-throughput sequencing technology.

Patients diagnosed with T2DM were enrolled as study subjects. Based on the presence of microvascular complications, subjects were divided into a study group, a control group. Clinical fecal samples from the two groups were subjected to diversity analysis using the Illumina MiSeq high-throughput sequencing technology, comparing the richness and diversity of the gut microbiota between the two groups. The Tax4Fun software was utilized for the functional prediction of differential microbiota.

A total of 3727 operational taxonomic units (OTUs) were identified, with 1311 OTUs common to both groups, and 1363 and 1053 OTUs unique to the study group and the control group, respectively. The study group exhibited a significant increase in the relative abundance of Clostridia and Negativicutes, and a marked decrease in Gammaproteobacteria, Bacilli, and Verrucomicrobia compared to the control group. LefSe analysis revealed significant differences in the relative abundance at two phyla, two classes, two orders, three families, and two genera levels between the groups. KEGG pathway analysis of differential microbiota identified 10 pathways with statistically significant differences (P<0.05).

This study reveals significant disparities in gut microbiota abundance between T2DM patients and those with microvascular complications of T2DM, suggesting potential microbial markers for diagnosing and treating microvascular complications of T2DM.

Intermittent fasting (IF) is an increasingly popular dietary approach involving alternating fasting and eating periods. This review aims to summarize the growing body of literature demonstrating that IF is a potential nutritional practice that involves alternating periods of fasting and eating and the numerous benefits of IF, especially in the modulation of healthy gut microbiota. The positive impact of intermittent fasting on gut microbiota not only promotes gastrointestinal health but also has far-reaching effects on critical systems throughout the body. Additionally, the evidence presented in this review highlights the significant preventive and therapeutic effects of intermittent fasting on a wide range of disorders. This includes reducing the risk of diabetes, and neurological disorders, alleviating obesity, and enhancing the functioning of the liver, ultimately contributing to the maintenance of metabolic equilibrium. Perhaps most notably, these effects play a substantial role in preventing diabetes, a global health concern of increasing significance. This comprehensive investigation delves into the scientific foundations of intermittent fasting's impact on gut microbiota and its implications for averting chronic diseases, providing valuable insights for future research and therapeutic applications.

Although low-dose lactulose has shown a good theoretical foundation for the treatment of ulcerative colitis (UC) in previous studies, the exact effects and mechanism remain unclear. The rats were randomly distributed into 5 groups, i.e., normal drinking water was provided for an initial 14 days in blank control group, 4% dextran sulfate sodium was used for modeling in the remaining 4 groups. During the 15-24th day, rats in the blank control group were administered with 0.9% saline (0.5 ml/d) by gavage. In the rest 4 groups, rats were administered 0.9% saline (0.5 ml/d, UC model), mesalazine (400 mg/kg/d), lactulose (1000 mg/kg/d), and lactulose + mesalazine (two-drug combination) by gavage. In addition to symptoms and pathological changes, serum IL-6, TNF-α, and High-sensitivity C-reactive protein(Hs-CRP) by ELISA analysis, mRNA and protein expression levels of TLR-2, TLR-4, Nuclear factor-κB(NF-κB), IL-6, and TNF-α in colon tissues by RT-qPCR and WB analyses respectively. Meanwhile, short-chain fatty acid(SCFAs) and intestinal flora were analyzed. Low-dose lactulose improved symptoms (diarrhea, blood in stool, weight loss) and pathological inflammation. In addition to serum IL-6, TNF-α, and Hs-CRP, the mRNA and protein expression levels of TLR-2, TLR-4, NF-κB, IL-6 and TNF-α in the colon were down-regulated with the intervention of lactulose.Meanwhile, lactulose decreased the ileocecal PH, increased SCFAs and altered the intestinal flora. Low-dose lactulose may be beneficial to UC by regulating TLRs/NF-κB pathway, reducing ileocecal PH, increasing SCFAs, regulating intestinal flora and improving the intestinal mucosal barrier. Meanwhile, low-dose lactulose and mesalazine may have additive effects upon combination.

Tongue-coating microbiota, especially known as the tongue microbiome, holds significant value as both a prospective clinical diagnostic biomarker and therapeutic target, which plays a crucial role in the oral microecological health. However, there is limited understanding of the composition and function of tongue coating microbiota in chronic kidney disease patients undergoing hemodialysis.

Thirty-one non-diabetic hemodialysis patients (nonDM_HD), 29 diabetic hemodialysis patients (DM_HD) and 33 healthy controls (HC) were enrolled. Swabs from tongue coating were collected. The 16S rDNA (V3-V4 region) was sequenced to scrutinize the tongue-coating bacterial microbiome difference.

Both nonDM_HD and DM_HD showed distinct bacterial communities of oral microbiota compared to HC. The abundance of Streptococcus, Lactobacillus, Ruminococcaceae G1, Ligilactobacillus and Abiotrophia showed a significant increase (p < 0.05) in DM_HD and nonDM_HD compared to HC, while Haemophilus, Lachnoanaerobaculum, Peptostreptococcaceae G1, Peptostreptococcus showed a significant decrease (p < 0.05) respectively. Veillonella, Lactobacillus, Limosilactobacillus etc. may serve as potential biomarkers for DM_HD. While Streptococcus, Ruminococcaceae G1, Actinobacillus, Abiotrophia can be considered alternative biomarkers for nonDM_HD. Moreover, the enriched Haemophilus, Actinomyces, Lachnoanaerobaculum were prominent features of the tongue coating microbiota in HC, which could be used as the potential therapeutic targets of chronic kidney disease. Network analysis revealed a less complex interaction relationship among the tongue coating bacterial microbiota of nonDM_HD and DM_HD. Furthermore, correlations were identified between the microbiome composition and clinical parameters of the individuals.

In conclusion, deciphering the tongue coating microbiota of kidney patients undergoing hemodialysis will helpful in assessing the role of oral microbiota in pathobiology and development of kidney disease, which is expected to become a potential biomarkers and adjuvant therapeutic target.

Short-chain fatty acids (SCFAs), primarily derived from gut microbiota, play a role in regulating fetal development; however, the mechanism remains unclear. Fetal SCFAs levels depends on maternal SCFAs transported via the placenta. Metabolic stress, particularly from diabetes and obesity, can disrupt maternal SCFAs levels, impairing fetal metabolic reprogramming. Dysregulated SCFAs may negatively impact the development of the fetal cardiovascular, nervous, and immune systems, potentially contributing to adverse outcomes in adulthood. This review focuses on recent advances regarding the role of maternal SCFAs in shaping the metabolic profile of offspring, especially in the context of various maternal metabolic disorders. Given that SCFAs may influence fetal development through the placenta-embryo axis, targeted SCFAs supplementation could be a promising strategy against developmental diseases associated with intrauterine risk factors.

There are limited longitudinal data from non-industrialized settings on patterns and determinants of gut bacterial microbiota development in early childhood. We analysed epidemiological data and stool samples collected from 60 children followed from early infancy to 5 years of age in a rural tropical district in coastal Ecuador. Data were collected longitudinally on a wide variety of individual, maternal, and household exposures. Extracted DNA from stool samples were analyzed for bacterial microbiota using 16S rRNA gene sequencing. Both alpha and beta diversity indices suggested stable profiles towards 5 years of age. Greater alpha diversity and lower beta diversity were associated with factors typical of rural poverty including low household incomes, overcrowding, and greater agricultural and animal exposures, but not with birth mode or antibiotic exposures. Consumption of unpasteurized milk was consistently associated with greater alpha diversity indices. Infants living in a non-industrialized setting in conditions of greater poverty and typically rural exposures appeared to acquire more rapidly a stable and diverse gut bacterial microbiome during childhood.

As next-generation sequencing technologies advance rapidly and the cost of metagenomic sequencing continues to decrease, researchers now face an unprecedented volume of microbiome data. This surge has stimulated the development of scalable microbiome data analysis methods and necessitated the incorporation of phylogenetic information into microbiome analysis for improved accuracy. Tools for constructing phylogenetic trees from 16S rRNA sequencing data are well-established, as the highly conserved regions of the 16S gene are limited, simplifying the identification of marker genes. In contrast, metagenomic and whole genome shotgun (WGS) sequencing involve sequencing from random fragments of the entire gene, making identification of consistent marker genes challenging owing to the vast diversity of genomic regions, resulting in a scarcity of robust tools for constructing phylogenetic trees. Although bacterial sequence tree construction tools exist for upstream bioinformatics, many downstream researchers-those integrating these trees into statistical models or machine learning-are either unaware of these tools or find them difficult to use due to the steep learning curve of processing raw sequences. This is compounded by the fact that public datasets often lack phylogenetic trees, providing only abundance tables and taxonomic classifications. To address this, we present a comprehensive review of phylogenetic tree construction techniques for microbiome data (16S rRNA or whole-genome shotgun sequencing). We outline the strengths and limitations of current methods, offering expert insights and step-by-step guidance to make these tools more accessible and widely applicable in quantitative microbiome data analysis.

Rice with high resistant starch (RS) exhibits the potential to improve glucose metabolism, insulin sensitivity. In this study, using two rice varieties-Samgwang, a medium-amylose rice, and Dodamssal, a high-amylose rice containing RS-we analyzed the composition and molecular structural characteristics of brown rice and its starch and the effects on fasting blood glucose levels, fecal short-chain fatty acid (SCFA), and gut microbiota after 8 weeks of consumption in mice. The amylose content of heat-treated Samgwang (HS) and -Dodamssal (HD) was 21.0 ± 0.2 and 47.5 ± 0.3 %, respectively, while RS contents were 0.8 ± 0.0 and 14.7 ± 1.0 %. HD exhibited a C-type starch crystallinity with a lower proportion of short chains and a higher proportion of long chains compared to HS. HD-fed mice exhibited lower fasting blood glucose levels and the highest SCFA levels in their feces. They also had the highest abundance of Ruminococcus bromii, an RS-degrading bacterium, the highest positive correlation with Faecalicatena fissicatena (r = 0.9), and the highest negative correlation with Lachnoclostridium scindens and Lawsonibacter asaccharolyticus (r = -0.8). Overall, HD consumption can improve glucose metabolism by increasing intestinal SCFA production and can serve as a prebiotic dietary ingredient to improve obesity and diabetes.

With the imbalance of intestinal microbiota, the body will then face an inflammatory response, which has serious implications for human health. Bodily allergies, injury or pathogens infections can trigger or promote inflammation and alter the intestinal environment. Meanwhile, excessive changes in the intestinal environment cause the imbalance of microbial homeostasis, which leads to the proliferation and colonization of opportunistic pathogens, invasion of the body's immune system, and the intensification of inflammation. Some natural compounds and gut microbiota and metabolites can reduce inflammation; however, the details of how they interact with the gut immune system and reduce the gut inflammatory response still need to be fully understood. The review focuses on inflammation and intestinal microbiota imbalance caused by pathogens. The body reacts differently to different types of pathogenic bacteria, and the ingestion of pathogens leads to inflamed gastrointestinal tract disorders or intestinal inflammation. In this paper, unraveling the interactions between the inflammation, pathogenic bacteria, and intestinal microbiota based on inflammation caused by several common pathogens. Finally, we summarize the effects of intestinal metabolites and natural anti-inflammatory substances on inflammation to provide help for related research of intestinal inflammation caused by pathogenic bacteria.

Fibroblast growth factor 21 (FGF21) is an important regulator of glycolipid metabolism. However, whether the gut microbiota is related to the anti-diabetic and obesity effects of FGF21 remains unclear.

Our research used KO/KO db/db male mice and streptozotocin (STZ)-induced to simulate the construction of two type II diabetic mellitus (T2DM) models, and detected impaired glucose tolerance in the model by using the ipGTT and ITT assays, and collected feces from the model mice for sequencing of the intestinal flora and the content of short-chain fatty acids. H＆E staining was used to detect changes in intestinal tissue, the serum levels of LPS and GLP-1 were detected by ELISA.

In this study, we found that FGF21 significantly improved insulin sensitivity, attenuated intestinal lesions, and decreased serum lipopolysaccharide (LPS) concentrations in T2DM mice. Moreover, FGF21 reshaped the gut microbiota and altered their metabolic pathways in T2DM mice, promoting the production of short-chain fatty acids (SCFAs) and the secretion of glucagon-like peptide 1 (GLP-1). Fecal transplantation experiments further confirmed that feces from FGF21-treated diabetic mice demonstrated similar effects as FGF21 in terms of anti-diabetic activity and regulation of gut microbiota dysbiosis. Additionally, the antibiotic depletion of gut microbiota abolished the beneficial effects of FGF21, including increased GLP-1 secretion and fecal SCFA concentration. Additionally, the FGF21 effects of ameliorating intestinal damage and suppressing plasma LPS secretion were suppressed. All these findings suggest that FGF21 prevents intestinal lesions by modifying the gut microbiota composition. Furthermore, FGF21 affected bile acid synthesis by inhibiting CYP7A1, the key enzyme of bile acid synthesis.

Therefore, FGF21 enriched beneficial bacteria by preventing bile acid synthesis and stimulating the secretion of the intestinal hormone GLP-1 via the increased production of gut microbiota metabolites, thereby exerting its anti-diabetic effects.

Selaginella tamariscina extracts (STS), total flavonoids of Selaginella tamariscina (TFST) and the main active component amentoflavone (AMT) have hypoglycaemic-mitigating effects, but their efficacy and mechanism of action in db/db mice are unknown. This study aimed to evaluate the hypoglycaemic effects of Selaginella tamariscina and its extracts in db/db diabetic mice and explore their mechanisms through gut microbiota modulation and metabolomics. Sixty male db/db mice were divided into model (db/db), STS (1.1 g/kg), TFST (140 mg/kg), AMT (60 mg/kg), mulberry twig alkaloid tablets (MTA, 24 mg/kg), and metformin (Met, 160 mg/kg) groups. Another 10 db/m mice served as controls. Treatments lasted 4 weeks. Blood glucose, body weight, diabetes symptoms, lipid levels, pathological changes, oxidative stress markers and liver damage levels were assessed. The gut microbiota composition was analyzed via 16S rDNA sequencing, and urinary metabolomics was conducted to understand metabolic changes. Selaginella tamariscina and its extracts significantly improved hyperglycaemia, insulin sensitivity, lipid metabolism, oxidative stress and liver injury in db/db mice, among which TFST was the most effective, with an effect comparable to that of Met and superior to that of MTA. TFST regulates gut microbiota disorders and metabolic profiles in db/db diabetic mice and modulates Alloprevotella levels, affecting butyric acid content and, thus, exerting a hypoglycaemic effect. These findings suggest that TFST modulates Alloprevotella, influencing butyric acid levels, which improves glycaemic control, enhances insulin sensitivity, and prevents oxidative stress and tissue damage. In conclusion, TFST has potential as a natural therapeutic agent for the control of T2DM.

The gut microbiota (GM), comprising trillions of microorganisms in the gastrointestinal tract, is a key player in the development of obesity and related metabolic disorders, such as type 2 diabetes (T2D), metabolic syndrome (MS), and cardiovascular diseases. This mini-review delves into the intricate roles and mechanisms of the GM in these conditions, offering insights into potential therapeutic strategies targeting the microbiota. The review elucidates the diversity and development of the human GM, highlighting its pivotal functions in host physiology, including nutrient absorption, immune regulation, and energy metabolism. Studies show that GM dysbiosis is linked to increased energy extraction, altered metabolic pathways, and inflammation, contributing to obesity, MS, and T2D. The interplay between dietary habits and GM composition is explored, underscoring the influence of diet on microbial diversity and metabolic functions. Additionally, the review addresses the impact of common medications and therapeutic interventions like fecal microbiota transplantation on GM composition. The evidence so far advocates for further research to delineate the therapeutic potential of GM modulation in mitigating obesity and metabolic diseases, emphasizing the necessity of clinical trials to establish effective and sustainable treatment protocols.

Polycystic ovary syndrome (PCOS) is one of the most common disorders among women in modern societies. A variety of factors can contribute to the development of PCOS. These women often exhibit high insulin resistance (IR), hyperandrogenism, irregular periods, and infertility. Dysbiosis of the gut microbiota (GMB) in women with PCOS has attracted the attention of many researchers. Porphyromonas spp., B. coprophilus, and F. prausnitzii are found in higher numbers in the gut of women with PCOS. Short-chain fatty acids (SCFAs), produced by the intestinal microbiota through fermentation, play an essential role in regulating metabolic activities and are helpful in reducing insulin resistance and improving PCOS symptoms. According to studies, the bacteria producing SCFAs in the gut of these women are less abundant than in healthy women. The effectiveness of using probiotic supplements has been proven to improve the condition of women with PCOS. Daily consumption of probiotics improves dysbiosis of the intestinal microbiome and increases the production of SCFAs.

The deleterious effects of human activities on biodiversity in the vegetal and animal world, and on climate changes are now well-established facts. However, little is yet known on the impact of human activities on microbial diversity on the planet and more specifically on the human microbiota Large implementation of metagenomics allows exaustive microbial cataloguing with broad spatio-temporal resolution of human microbiota. A reduction in bacterial richness and diversity in the human microbiota, particularly in the intestinal tract, is now established and particularly obvious in the most industrialized regions of the planet. Massive, uncontrolled use of antibiotics, drastic changes in traditional food habits and some elements of the "global exposome" that remain to identify are usually considered as stressors accounting for this situation of "missing microbes". As a consequence, a dysbiotic situation develops, a "dysbiosis" being characterized by the erosion of the central core of shared bacterial species across individuals and the development of opportunistic "pathobionts" in response to a weaker barrier capacity of these impoverished microbiota. The current challenge is to establish a causality link between the extension of these dysbiotic situations and the steady emergence of epidemic, non-communicable diseases such as asthma, allergy, obesity, diabetes, autoimmune diseases and some cancers. Experimental animal models combined with controlled, prospective clinical interventions are in demand to consolidate causality links, with the understanding that in the deciphering of the mechanisms of alteration of the human-microbiome symbiosis resides a novel exciting chapter of medicine: "microbial medicine".

In recent years, in-depth research has revealed that gut microbiota has an inseparable relationship with erectile dysfunction (ED) in men.

(1) To review the correlation between gut microbiota and ED from the perspective of its impact on men's mental health, metabolism, immunity, and endocrine regulation and (2) to provide reference to further explore the pathogenesis of ED and the improvement of clinical treatment plans.

PubMed was used for the literature search to identify publications related to ED and gut microbiota.

Gut microbiota may induce depression and anxiety through the microbiota-gut-brain axis, leading to the occurrence of psychological ED. It may also cause vascular endothelial dysfunction and androgen metabolism disorder by interfering with lipid metabolism, immunity, and endocrine regulation, leading to the occurrence of organic ED.

Gut microbiota and its metabolites play an important role in the occurrence and development of ED. As a new influencing factor of ED, gut microbiota disorder is expected to become a target for treatment.

Type 2 diabetes (T2D) is a metabolic disease characterized by chronic hyperglycemia because of insulin resistance (IR) and\or pancreatic β-cell dysfunction. Last century research showed that gut microbiota has a direct effect on metabolism and metabolic diseases. New studies into the human microbiome and its connection with the host is making it possible to develop new therapies for a wide variety of diseases. Inflammation is a well-known precursor to metabolic syndrome, which increases the risk of hypertension, visceral obesity, and dyslipidemia, which can lead to T2D through the damage of pancreatic β-cell and reduce insulin secretion. Current understanding for beneficial effects of probiotics in T2D strictly rely on both animal and clinical data, which mostly focused on their impact on IR, anthropometric parameters, glycemic control and markers of chronic systemic inflammation. From the other hand, there is a lack of evidence-based probiotic efficacy on pancreatic β-cell function in terms of T2D and related metabolic disorders. Therefore, current review will focus on the efficacy of probiotics for the protection of β-cells damage and it`s mechanism in patients with T2D.

Metabolic syndrome (MetS), characterized by obesity, hyperglycemia, and abnormal blood lipid levels, is the pathological basis of many cardiovascular diseases. Gualou-Xiebai-Banxia-Tang decoction (GT) was first described in the Synopsis of the Golden Chamber, the earliest traditional Chinese medicine (TCM) monograph on diagnosis and treatment of miscellaneous diseases in China. According to TCM precepts, based on its ability to activate yang to release stagnation, activate qi to reduce depression, remove phlegm, and broaden the chest, GT has been used for more than 2,000 years to treat cardiovascular ailments. However, the molecular bases of its therapeutic mechanisms remain unclear.

The aim of this study was to identify lipid- and glucose-related hepatic genes differentially regulated by GT, and to assess GT impact on gut microbiota composition, in mice with high-fat diet (HFD)-induced MetS.

ApoE-/- mice were fed with an HFD for 24 weeks, with or without concurrent GT supplementation, to induce MetS. At the study's end, body weight, visceral fat weight, blood lipid levels, and insulin sensitivity were measured, and histopathological staining was used to evaluate hepatosteatosis and intestinal barrier integrity. Liver transcriptomics was used for analysis of differentially expressed genes in liver and prediction of relevant regulatory pathways. Hepatic lipid/glucose metabolism-related genes and proteins were detected by RT-qPCR and western blotting. Gut microbial composition was determined by 16S rRNA gene sequencing.

GT administration reduced MetS-related liver steatosis and weight gain, promoted insulin sensitivity and lipid metabolism, and beneficially modulated gut microbiota composition by decreasing the relative abundance of g_Lachnospiraceae_NK4A136_group and increasing the relative abundance of g_Alistipes. Liver transcriptomics revealed that GT regulated the expression of genes related to lipid and glucose metabolism (Pparγ, Igf1, Gpnmb, and Trem2) and of genes encoding chemokines/chemokine receptors (e.g. Cxcl9 and Cx3cr1). Significant, positive correlations were found for Ccr2, Ccl4, Ccr1, and Cx3cr1 and the g_Lachnospiraceae_NK4A136_group, and between Cxcl9, Ccr2, Ccl4, and Cx3cr1 and g_Desulfovibrio. GT treatment downregulated the protein expressions of SCD1 and CX3CR1 and upregulated the expression of PCK1 protein.

GT supplementation alleviates HFD-induced MetS in mice by improving hepatic lipid and glucose metabolism. The anti-metabolic syndrome effects of GT may be related to the regulation of the gut-liver axis.

The plant Smilax china L., also known as Jingangteng, is suspected of regulating glucose and lipid metabolism. Jingangteng capsules (JGTCs) are commonly used to treat gynecological inflammation in clinical practice. However, it is not clear whether JGTCs can regulate glucose and lipid metabolism, and the mechanism is unclear.

To investigate the impact and mechanism of action of JGTCs on diabetes and liver lipid disorders in rats.

The chemical constituents of JGTCs were examined using ultra-high-performance liquid chromatography with quadrupole time-of-flight mass spectrometry. A high-fat diet and streptozotocin-induced diabetes model was used to evaluate anti-diabetic effects by assessing blood glucose and lipid levels and liver function. The mechanism was explored using fecal 16S rRNA gene sequencing and metabolomics profiling, reverse transcription-quantiative polymerase chain reaction (RT-qPCR), and Western blot analysis.

Thirty-three components were identified in JGTCs. The serological and histomorphological assays revealed that JGTC treatment reduced levels of blood glucose and lipids, aspartate aminotransferase, alanine aminotransferase, and lipid accumulation in the liver of diabetic rats. According to 16S rDNA sequencing, JGTCs improved species richness and diversity in diabetic rats' intestinal flora and restored 22 dysregulated bacteria to control levels. Fecal metabolomics analysis showed that the altered fecal metabolites were rich in metabolites, such as histidine, taurine, low taurine, tryptophan, glycerophospholipid, and arginine. Serum metabolomics analysis indicated that serum metabolites were enriched in the metabolism of glycerophospholipids, fructose and mannose, galactose, linoleic acid, sphingolipids, histidine, valine, leucine and isoleucine biosynthesis, and tryptophan metabolism. Heatmaps revealed a strong correlation between metabolic parameters and gut microbial phylotypes. Molecular biology assays showed that JGTC treatment reversed the decreased expression of farnesoid X receptor (FXR) in the liver of diabetic rats and inhibited the expression of lipogenic genes (Srebp1c and FAS) as well as inflammation-related genes (interleukin (IL)-β, tumor necrosis factor (TNF)-α, and IL-6). Liver metabolomics analysis indicated that JGTC could significantly regulate a significant number of bile acid metabolites associated with FXR, such as glyco-beta-muricholic acid, glycocholic acid, tauro-beta-muricholic acid, and tauro-gamma-muricholic acid.

This was the first study to investigate the mechanisms of JGTCs' effects on liver lipid disorders in diabetic rats. JGTCs inhibited liver lipid accumulation and inflammatory responses in diabetic rats by affecting intestinal flora and metabolic disorders and regulating FXR-fat synthesis-related pathways to alleviate diabetic lipid disorders.

Over recent years, the scientific community has acknowledged the crucial role of certain microbial strains inhabiting the intestinal ecosystem in promoting human health, and participating in various beneficial functions for the host. These microorganisms are now referred to as next-generation probiotics and are currently considered as biotherapeutic products and food or nutraceutical supplements. However, the majority of next-generation probiotic candidates pose nutritional demands and exhibit high sensitivity towards aerobic conditions, leading to numerous technological hurdles in large-scale production. This underscores the need for the development of suitable delivery systems capable of enhancing the viability and functionality of these probiotic strains. Currently, potential candidates for next generation probiotics (NGP) are being sought among gut bacteria linked to health, which include strains from the genera Bacteroids, Faecalibacterium, Akkermansia and Clostridium. In contrast to Lactobacillus spp. and Bifidobacterium spp., NGP, particularly Bacteroids spp. and Clostridium spp., appear to exhibit greater ambiguity regarding their potential to induce infectious diseases. The present review provides a comprehensive overview of NGPs in terms of their health beneficial effects, regulation framework and risk assessment targeting relevant criteria for commercialization in food and pharmaceutical markets.

Diabetes mellitus (DM) is more common among people living with human immunodeficiency virus (PLWH) compared with healthy individuals. In a prospective multicenter study (N = 248), we identified normoglycemic (48.7%), prediabetic (44.4%), and diabetic (6.9%) PLWH. Glycosylated hemoglobin (HbA1c) and fasting blood glucose (FBG) sensitivity in defining dysglycemia was 96.8%, while addition of oral glucose tolerance test led to reclassification of only 4 patients. Inclusion of 93 additional PLWH with known DM enabled identification of multiple independent predictors of dysglycemia or diabetes: older age, higher body mass index, Ethiopian origin, HIV duration, lower integrase inhibitor exposure, and advanced disease at diagnosis. Shotgun metagenomic microbiome analysis revealed 4 species that were significantly expanded with hyperglycemia/hyperinsulinemia, and 2 species that were differentially more prevalent in prediabetic/diabetic PLWH. Collectively, we uncover multiple potential host and microbiome predictors of altered glycemic status in PLWH, while demonstrating that FBG and HbA1c likely suffice for diabetes screening. These potential diabetic predictors merit future prospective validation.

Polyphenols in mulberry fruit have potential anti-diabetic effects by targeting the gut microbiota. This study investigated how mulberry polyphenols (MPs) influence the microbiota of the small and large intestines and their effects on type 2 diabetes symptoms. The results showed lower microbiota densities in the small intestine. MP treatments improved microbiota richness and diversity in both intestines, similar to metformin. In particular, at a 400 mg kg-1 dose, mulberry polyphenols decreased Firmicutes, Lactobacillus, and Bacilli, while increasing Bacteroidetes, leading to elevated propionate and butyrate levels. Less abundant small intestinal microbiota, like Enterobacterales, Mycoplasmatales, Enterobacteriaceae, and Ureaplasma, were involved in regulating blood glucose and insulin levels. Functional analysis suggested that mulberry polyphenols reshaped the small intestinal microbiota to influence blood glucose balance via unknown pathways, while in the large intestine, they primarily affected blood glucose through carbohydrate transport and metabolism. Based on their ability to regulate the composition of intestinal flora, MPs likely improved glucose homeostasis by enhancing glucose utilization, supporting pancreatic tissue health, and increasing serum antioxidant capacity. However, the specific mechanisms underlying this potential are yet to be fully explored. This study provides new insights into the influence of MPs on remodeling the microbiota residing in both the small and large intestines, which thereby may contribute to the improvement of the pathophysiology of type 2 diabetes.

It has been four years since long COVID-the protracted consequences that survivors of COVID-19 face-was first described. Yet, this entity continues to devastate the quality of life of an increasing number of COVID-19 survivors without any approved therapy and a paucity of clinical trials addressing its biological root causes. Notably, many of the symptoms of long COVID are typically seen with advancing age. Leveraging this similarity, we posit that Geroscience-which aims to target the biological drivers of aging to prevent age-associated conditions as a group-could offer promising therapeutic avenues for long COVID. Bearing this in mind, this review presents a translational framework for studying long COVID as a state of effectively accelerated biological aging, identifying research gaps and offering recommendations for future preclinical and clinical studies.

The evolution of the gut-microbiota-brain axis in animals reveals that microbial inputs influence metabolism, the regulation of inflammation and the development of organs, including the brain. Inflammatory, neurodegenerative and psychiatric disorders are more prevalent in people of low socioeconomic status (SES). Many aspects of low SES reduce exposure to the microbial inputs on which we are in a state of evolved dependence, whereas the lifestyle of wealthy citizens maintains these exposures. This partially explains the health deficit of low SES, so focussing on our evolutionary history and on environmental and lifestyle factors that distort microbial exposures might help to mitigate that deficit. But the human microbiota is complex and we have poor understanding of its functions at the microbial and mechanistic levels, and in the brain. Perhaps its composition is more flexible than the microbiota of animals that have restricted habitats and less diverse diets? These uncertainties are discussed in relation to the encouraging but frustrating results of attempts to treat psychiatric disorders by modulating the microbiota.

The gut microbiota, amounting to approximately 100 trillion (1014) microbes represents a genetic repertoire that is bigger than the human genome itself. Evidence on bidirectional interplay between human and microbial genes is mounting. Microbiota probably play vital roles in diverse aspects of normal human metabolism, such as digestion, immune modulation, and gut endocrine function, as well as in the genesis and progression of many human diseases. Indeed, the gut microbiota has been most closely linked to various chronic ailments affecting the liver, although concrete scientific data are sparse. In this narrative review, we initially discuss the basic epidemiology of gut microbiota and the factors influencing their initial formation in the gut. Subsequently, we delve into the gut-liver axis and the evidence regarding the link between gut microbiota and the genesis or progression of various liver diseases. Finally, we summarise the recent research on plausible ways to modulate the gut microbiota to alter the natural history of liver disease.

L-Arabinose, lactulose, and Lactobacillus plantarum (L. plantarum) have been reported to have glucolipid-lowering effects. Here, the effects of L-arabinose and lactulose combined with L. plantarum on obesity traits were investigated. According to the experimental results, the combination of L-arabinose, lactulose, and L. plantarum was more effective at reducing body weight, regulating glucolipid metabolism, and improving insulin resistance. Besides, this combination showed immunomodulatory activity by adjusting the T lymphocyte subsets and reduced the immune-related cytokine production. Moreover, it improved the gut barrier, ameliorated the disorder of gut microbiota, and upregulated the levels of SCFAs. More importantly, the AL group, LP group, and ALLP group showed different regulatory effects on the abundance of Bifidobacterium and Lactobacillus due to the presence of lactulose and L. plantarum. These findings elucidate that the combination of L-arabinose, lactulose, and L. plantarum constitutes a new synbiotic combination to control obesity by modulating glucolipid metabolism, immunomodulatory activity, inflammation, gut barrier, gut microbiota and production of SCFAs.

Polysaccharides from Pinelliae Rhizoma Praeparatum Cum Alumine (PPA) have various biological activities, but their properties after oral administration are not clear. In this study, the absorption, digestion and fermentation properties of PPA were studied using in vivo fluorescence tracking, in vitro simulated digestion and fecal fermentation experiments. The absorption experiment showed that fluorescence was only observed in the gastrointestinal system, indicating that PPA could not be absorbed. Simulated digestion results showed that there were no significant changes in the molecular weight, Fourier transform infrared spectroscopy (FT-IR) spectrum, monosaccharides and reducing sugar of PPA during the digestion process, showing that the overall structure of PPA was not damaged. However, the carbohydrate gel electrophoresis bands of PPA enzymatic hydrolysates after simulated digestion were significantly changed, indicating that simulated digestion might impact the configuration of PPA. In vitro fermentation showed that PPA could be degraded by microorganisms to produce short chain fatty acids, leading to a decrease in pH value. PPA can promote the proliferation of Bacteroideaceae, Megasphaera, Bacteroideaceae, and Bifidobacteriaceae, and inhibit the growth of Desulfobacteriota and Enterobacteriaceae. The results indicated that PPA could treat diseases by regulating gut microbiota, providing a scientific basis for the application and development of PPA.

With genetic information gained from next-generation sequencing (NGS) and genome-wide association studies (GWAS), it is now possible to select for genes that encode reporter molecules that may be used to detect abnormalities such as alcohol-related liver disease (ARLD), cancer, cognitive impairment, multiple sclerosis (MS), diabesity, and ischemic stroke (IS). This, however, requires a thorough understanding of the gut-brain axis (GBA), the effect diets have on the selection of gut microbiota, conditions that influence the expression of microbial genes, and human physiology. Bacterial metabolites such as short-chain fatty acids (SCFAs) play a major role in gut homeostasis, maintain intestinal epithelial cells (IECs), and regulate the immune system, neurological, and endocrine functions. Changes in butyrate levels may serve as an early warning of colon cancer. Other cancer-reporting molecules are colibactin, a genotoxin produced by polyketide synthetase-positive Escherichia coli strains, and spermine oxidase (SMO). Increased butyrate levels are also associated with inflammation and impaired cognition. Dysbiosis may lead to increased production of oxidized low-density lipoproteins (OX-LDLs), known to restrict blood vessels and cause hypertension. Sudden changes in SCFA levels may also serve as a warning of IS. Early signs of ARLD may be detected by an increase in regenerating islet-derived 3 gamma (REG3G), which is associated with changes in the secretion of mucin-2 (Muc2). Pro-inflammatory molecules such as cytokines, interferons, and TNF may serve as early reporters of MS. Other examples of microbial enzymes and metabolites that may be used as reporters in the early detection of life-threatening diseases are reviewed.

Polycystic ovary syndrome (PCOS) is a common systemic disorder related to endocrine disorders, affecting the fertility of women of childbearing age. It is associated with glucose and lipid metabolism disorders, altered gut microbiota, and insulin resistance. Modern treatments like pioglitazone, metformin, and spironolactone target specific symptoms of PCOS, while in Chinese medicine, moxibustion is a common treatment. This study explores moxibustion's impact on PCOS by establishing a dehydroepiandrosterone (DHEA)-induced PCOS rat model. Thirty-six specific pathogen-free female Sprague-Dawley rats were divided into four groups: a normal control group (CTRL), a PCOS model group (PCOS), a moxibustion treatment group (MBT), and a metformin treatment group (MET). The MBT rats received moxibustion, and the MET rats underwent metformin gavage for two weeks. We evaluated ovarian tissue changes, serum testosterone, fasting blood glucose (FBG), and fasting insulin levels. Additionally, we calculated the insulin sensitivity index (ISI) and the homeostasis model assessment of insulin resistance index (HOMA-IR). We used 16S rDNA sequencing for assessing the gut microbiota, 1H NMR spectroscopy for evaluating metabolic changes, and Spearman correlation analysis for investigating the associations between metabolites and gut microbiota composition. The results indicate that moxibustion therapy significantly ameliorated ovarian dysfunction and insulin resistance in DHEA-induced PCOS rats. We observed marked differences in the composition of gut microbiota and the spectrum of fecal metabolic products between CTRL and PCOS rats. Intriguingly, following moxibustion intervention, these differences were largely diminished, demonstrating the regulatory effect of moxibustion on gut microbiota. Specifically, moxibustion altered the gut microbiota by increasing the abundance of UCG-005 and Turicibacter, as well as decreasing the abundance of Desulfovibrio. Concurrently, we also noted that moxibustion promoted an increase in levels of short-chain fatty acids (including acetate, propionate, and butyrate) associated with the gut microbiota of PCOS rats, further emphasizing its positive impact on gut microbes. Additionally, moxibustion also exhibited effects in lowering FBG, testosterone, and fasting insulin levels, which are key biochemical indicators associated with PCOS and insulin resistance. Therefore, these findings suggest that moxibustion could alleviate DHEA-induced PCOS by regulating metabolic levels, restoring balance in gut microbiota, and modulating interactions between gut microbiota and host metabolites.

The nasal cavity is the initial site of the human respiratory tract and is one of the habitats where microorganisms colonize. The findings from a growing number of studies have shown that the nasal microbiome is an important factor for human disease and health. 16S rRNA sequencing and metagenomic next-generation sequencing (mNGS) are the most commonly used means of microbiome evaluation. Among them, 16S rRNA sequencing is the primary method used in previous studies of nasal microbiomes. However, neither 16S rRNA sequencing nor mNGS can be used to analyze the genes specifically expressed by nasal microorganisms and their functions. This problem can be addressed by proteomic analysis of the nasal microbiome.

In this review, we summarize current advances in research on the nasal microbiome, introduce the methods for proteomic evaluation of the nasal microbiome, and focus on the important roles of proteomic evaluation of the nasal microbiome in the diagnosis and treatment of related diseases.

The detection method for microbiome-expressed proteins is known as metaproteomics. Metaproteomic analysis can help us dig deeper into the nasal microbiomes and provide new targets and ideas for clinical diagnosis and treatment of many nasal dysbiosis-related diseases.