Chronic atrophic gastritis (CAG) is a pivotal precancerous condition in gastric carcinogenesis, with progression typically following the classic Correa cascade. Although Helicobacter pylori (H. pylori) infection is widely recognized as the principal etiological factor, the persistence of gastric cancer (GC) risk in a subset of patients after successful eradication suggests that gastric microbiota dysbiosis may also contribute to CAG progression. In recent years, high-throughput sequencing technologies have revealed distinct microbial restructuring in patients with CAG, characterized by decreased microbial diversity, depletion of commensal taxa, and enrichment of opportunistic pathogens. These compositional changes are accompanied by metabolic dysfunction, activation of inflammatory signaling pathways, and disruption of immune homeostasis, which may contribute to a microenvironment permissive for precancerous transformation of the gastric mucosa. Probiotics and related microbiome-based therapeutics, including prebiotics, synbiotics, and postbiotics, have emerged as promising adjunctive strategies for H. pylori eradication and disease management. Their beneficial effects are mediated through multiple mechanisms, including remodeling of the microbial community, inhibition of pathogen colonization, modulation of host immune responses, and restoration of mucosal barrier integrity. However, whether these interventions can reverse established atrophic or metaplastic lesions remains unclear. In addition, how strain specificity, dose dependency, and interindividual heterogeneity influence clinical efficacy has yet to be fully elucidated. In this review, we summarize the compositional and functional features of gastric microbiota dysbiosis in patients with CAG, as well as the mechanisms and clinical applications of microbiome-based interventions. We further highlight current limitations in the field and discuss future directions for precision microecological therapies integrating multi-omics approaches, engineered probiotics, and artificial intelligence. These advances may provide a theoretical framework and practical guidance for the diagnosis and management of CAG and the prevention of GC.

The gut-mammary gland axis connects the communication between the gut microbiota and the mammary gland.Studies have reported that dysbiosis in gut microbiota is involved in the pathogenesis of breast diseases such as mastitis and breast cancer.In addition,different diets,including the supplementation of probiotics or prebiotics,which are closely related to the alteration of gut microbiota,were found to affect the nutritional contents of human milk and contribute to the development or alleviation of breast diseases.These studies suggested that the gut microbiota might be a new target for the regulation of human milk components or breast diseases.In this article,we summarized recent research advances in the gut-mammary gland axis and discussed some of the effective mechanisms and pathways involved,including distal translocation of gut microbiota,circulation of metabolites across the blood-milk barrier,the delivery of immune cells and their secreted antibodies to the mammary gland.This article also provides new strategies for preventing women's breast diseases and improving the composition of human milk through the gut-mammary axis.

Gut microbiota dysbiosis is intricately linked to metabolic disorders such as obesity, type 2 diabetes mellitus (T2DM), hyperlipidemia, and non-alcoholic fatty liver disease (NAFLD). Traditional Chinese medicine (TCM), particularly when combined with probiotic fermentation, offers a promising therapeutic strategy by modulating microbial balance and host metabolism. This narrative review synthesizes current research on probiotic-fermented herbal bioactives, focusing on their mechanisms in ameliorating metabolic diseases. Probiotic and bioactive compounds (e.g., berberine, polysaccharides) are highlighted for their roles in enhancing intestinal barrier function, regulating microbial metabolites like short-chain fatty acids (SCFAs), and reducing inflammation. Fermentation techniques improve the bioavailability of TCM components while reducing toxicity, as seen in fermented Salvia miltiorrhiza and Rhizoma Coptidis. Despite promising results, challenges include the complexity of microbiota–host interactions and variability in TCM standardization. Future directions emphasize integrating multi-omics technologies and personalized approaches to optimize probiotic-fermented TCM therapies. This review underscores the potential of combining traditional herbal wisdom with modern biotechnology to address metabolic disorders, which pose significant global health challenges, through a “gut microbiota–metabolism” axis. Emerging evidence highlights the critical role of gut microbiota dysbiosis in the pathogenesis of these conditions. TCM has shown promise in modulating gut microbiota to restore metabolic homeostasis. This review synthesizes current research on TCM-derived interventions, such as herbal compounds, probiotics, and fermentation techniques, that target gut microbiota to ameliorate metabolic disorders. We discuss mechanisms of action, including prebiotic effects, enhancement of intestinal barrier function, and regulation of microbial metabolites, while addressing the limitations and future directions of TCM-based therapies.

IntroductionTraditional Chinese Medicine (TCM) classifies botanical drugs based on their thermal properties (an emic classification system), categorizing them as “cold” (e.g., “clearing heat” for anti-inflammatory effects) or “hot” (e.g., “warming the middle” for metabolic enhancement). However, the specific roles of these botanical drugs in restoring gut microbiota dysbiosis remain unclear. This study aimed to explore whether TCM-classified cold and hot botanical drugs differentially restore gut microbiota dysbiosis and host physiology in antibiotic-treated mice.MethodsMice with antibiotic-induced dysbiosis were treated with eight TCM-classified botanical drugs (four cold: Rheum palmatum L., Scutellaria baicalensis Georgi, Senna alexandrina Mill., Coptis chinensis Franch.; four hot: Codonopsis pilosula (Franch.) Nannf., Astragalus membranaceus (Fisch.) Bunge, Angelica sinensis (Oliv.) Diels, Panax ginseng C.A.Mey.) for 20 days. Gut microbiota were analyzed via 16S rRNA sequencing on days 5, 10, 15, and 20, alongside physiological parameters including blood glucose, serum lipids, TNF-α, adiponectin, and intestinal histomorphology.ResultsBy day 20, all botanical drugs restored the diversity and ranking of dominant genera (those with >10% abundance, such as Lactobacillus and unclassified Muribaculaceae). However, cold-classified drugs, traditionally associated with anti-inflammatory effects, selectively enriched anti-inflammatory taxa, including Akkermansia and Bifidobacterium. In contrast, hot-classified drugs, linked to metabolic enhancement, promoted metabolic-modulating genera such as Clostridia and Eubacterium coprostanoligenes. These differential enrichments corresponded with the therapeutic principles defined by TCM: cold-classified drugs reduced serum TNF-α levels (P < 0.01), demonstrating anti-inflammatory effects, whereas hot-classified drugs improved lipid profiles (TG: P < 0.001), thereby promoting metabolic modulation.DiscussionTCM-classified cold and hot botanical drugs universally stabilize dominant microbiota while differentially modulating low-abundance taxa. The enrichment of Akkermansia (cold) and Clostridia (hot) offers a microbiota-driven validation of TCM’s empirical classification framework. These findings connect traditional knowledge with microbial ecology, underscoring the potential of TCM-guided microbiota modulation for precision therapies.

Helicobacter pylori infection, affecting over 4.4 billion individuals globally, is a leading cause of chronic gastritis, peptic ulcers and gastric cancer. At present, the standard therapeutic approach for H. pylori infection continues to rely on high-dose antibiotic regimens, despite growing concerns about antibiotic resistance and treatment-associated dysbiosis. Probiotics, particularly Lactobacillus species, have emerged as promising adjuncts due to their multifaceted anti- H. pylori mechanisms. However, only a limited number of existing strains have demonstrated efficacy in treating H. pylori infections. This study investigated the effects of Lactiplantibacillus plantarum HCS03-001 (LP-HCS03) and Lacticaseibacillus paracasei HCS17-040 (LPC-HCS17) against H. pylori using a mouse model. In infected mice, administration of the combined probiotics with 1 × 10 9 CFU each significantly decreased mRNA expression levels of ureA/ureB ( P < 0.001), increased the level of IL-10, and decreased the levels of IL-17 and TNF-α ( P < 0.001), which indicates that the intervention reduced gastric colonization, alleviated inflammation and promoted the restoration of the gastric mucosal barrier. The microbiota in both the stomach and intestines were reconstructed, with particularly pronounced effects observed in the stomach. These findings highlight LP-HCS03 and LPC-HCS17 as promising probiotics to augment H. pylori eradication while preserving microbial homeostasis.

BACKGROUND:Hyperuricemia (HU), characterized by elevated serum uric acid (UA) levels, is associated with metabolic disorders, renal diseases, gout and gut dysbiosis. Withania coagulans (WC) and Fagonia cretica (FC) are medicinal plants traditionally used in Pakistan for their antioxidant and anti-inflammatory properties; however, their potential in HU management remains unexplored. PURPOSE:This study investigates the efficacy of WC and FC crude extracts in ameliorating HU and explores the underlying mechanisms in mice models with HU. METHODS:Liquid chromatography and mass spectrometry (LC-MS) were adopted to characterize the major components within the crude extracts of WC and FC. HU was induced in BALB/c mice using potassium oxonate (PO) and adenine (A) for 21 days. Mice models were treated orally with WC (200mg/kg) and FC (200mg/kg) crude extracts during HU induction. Serum UA, creatinine, and inflammatory markers were analyzed using ELISA. The molecular expression of UA transporters (ABCG2 and SLC2A9) and TLR4/MyD88/NF-κB pathway components were assessed via qRT-PCR and immunoblotting. Gut microbiota composition was analyzed via fecal 16S rRNA sequencing, and metabolomic profiling identified key metabolites. In vitro studies were conducted using Hep G2 and HT-29 cells to examine the effects of gut microbiota-derived metabolites on xanthine oxidase (XOD) activity and UA transporters. RESULTS:Treatment with WC and FC markedly lowered serum UA, creatinine, and hepatic inflammatory cytokine levels in HU mice. WC showed strong effects in inhibiting XOD activity, while FC significantly upregulated intestinal UA transporters, suggesting their different mechanisms of action. WC and FC treatment reduced pro-inflammatory cytokines (IL-1β, TNF-α, IL-6, IL-18) and LPS levels via downregulating the TLR4/MyD88/NF-κB pathway, indicating a strong anti-inflammatory effect. Additionally, the anti-inflammatory cytokine IL-10 was markedly increased. WC extracts restored gut microbial diversity by increasing the levels of Bifidobacterium, while FC increased Eubacterium xylanophilum. Metabolomic analysis of the gut microbiota revealed increased spermidine (SP) levels in WC-treated mice and traumatic acid (TA) levels in FC-treated mice, which contributed to reduced UA synthesis and enhanced excretion. In vitro cell-line and transcriptomic analyses demonstrated that key metabolites, SP (showing XOD inhibition) and TA (enhancing UA excretion), alleviated liver and intestinal dysfunction by suppressing TNF and IL-17 signaling pathways. The combined treatment exhibited synergistic effects. CONCLUSION:This study highlights the complementary mechanisms of Withania coagulans (WC) and Fagonia cretica (FC) in managing hyperuricemia (HU). WC primarily inhibits xanthine oxidase (XOD), reducing uric acid (UA) synthesis, while FC enhances UA excretion by upregulating transporters ABCG2 and SLC2A9. The WC extract alleviated PO+A-induced HU through its anti-inflammatory properties and modulation of gut microbiota-derived SP production, leading to XOD inhibition by suppressing the TNF signaling pathway. Similarly, the FC extract exhibited anti-inflammatory effects and modulated TA production, promoting UA exporters (Abcg2/Slc2a9) and enhancing intestinal UA excretion by suppressing the IL-17 signaling pathway. The combination of WC and FC synergistically reduces UA levels by both inhibiting XOD and promoting UA excretion. These results support the potential of WC and FC as natural therapeutic agents for HU management.

Probiotic fermentation can promote the release of more effective components from traditional Chinese medicines (TCMs). Astragalus membranaceus (Fisch.) Bunge (A. membranaceus) and Raphani Semen are TCMs that have gained attention for their immunoenhancing activities. This study aimed to investigate the effects and underlying mechanisms of probiotic-fermented A. membranaceus and Raphani Semen (PROAS) in cyclophosphamide (CTX)-induced immunocompromised mice. Changes in the composition of A. membranaceus and Raphani Semen after fermentation by probiotic strains, including Bifidobacterium longum SD5219, Lactobacillus fermentum NCIMB5221, and Lactobacillus paracasei SD5219, were identified using high-performance liquid chromatography. The immunostimulatory effects and mechanisms of PROAS were evaluated in immunosuppressed mice 3 and 7 days after CTX treatment. Probiotic fermentation of TCMs resulted in changes in major bioactive components. PROAS supplementation effectively restored intestinal integrity in CTX-treated mice by upregulating the mRNA expression of the tight junction proteins. PROAS significantly ameliorated the reduction in the spleen index and number of B lymphocytes caused by CTX treatment and regulated the secretion of cytokines in serum and colon tissues. PROAS administration modulated gut microbial dysbiosis and short-chain fatty acid (SCFA) content in CTX-treated mice. These results suggest that PROAS enhances B lymphocyte function by increasing the regulation of intestinal microbiota to produce high levels of SCFA, repairs the intestinal barrier damage induced by CTX, and promotes intestinal mucosal immunity.

Probiotics such as Lactobacillus and Bifidobacterium spp. have been shown to be critical for maintaining host homeostasis. In recent years, key compounds of postbiotics derived from probiotic metabolism and cellular secretion have been identified for their role in maintaining organ immunity and regulating intestinal inflammation. In particular, probiotic-derived extracellular vesicles (PEVs) can act as postbiotics, maintaining almost the same functional activity as probiotics. They also have strong biocompatibility and loading capacity to carry exogenous or parental active molecules to reach distal organs to play their roles. This provides a new direction for understanding the intrinsic microbiota-host communication mechanism. However, most current studies on PEVs are limited to their functional effects/benefits, and their specific physicochemical properties, composition, intrinsic mechanisms for maintaining host homeostasis, and possible threats remain to be explored. Here, we review and summarize the unique physicochemical properties of PEVs and their bioactivities and mechanisms in mediating microbiota-host communication, and elucidate the limitations of the current research on PEVs and their potential application as postbiotics.

ABSTRACT Human milk oligosaccharides (HMOs) are bioactive components pivotal for infant health, whose biosynthesis is modulated by intrinsic (genetic, metabolic) and extrinsic (diet, microbiota) maternal factors. Emerging evidence suggests the gut microbiota regulates HMO production through the gut–mammary axis, but mechanistic understanding remains fragmentary. Here, we investigated how gestational and postpartum gut dysbiosis induced by dextran sulfate sodium (DSS) disrupts milk oligosaccharide (MO) synthesis in mice and explored whether targeted probiotic supplementation could counteract lactation insufficiency under dysbiotic conditions. These results revealed that DSS‐exposed dams exhibited gut barrier disruption and systemic inflammation, accompanied by a significant reduction in mammary sialylated oligosaccharides (particularly 3′‐sialyllactose, 3′‐SL) and compromised blood–milk barrier integrity. Through integrated analysis of gut/milk microbiota and host parameters, we identified gut‐derived lipopolysaccharide (LPS) as a key mediator suppressing mammary glycosyltransferase genes critical for lactose synthesis and sialylation. LPS treatment of human mammary epithelial cells (MCF‐10A) recapitulated these effects, confirming direct transcriptional repression. Systematic in vitro screening of 15 probiotic strains identified three candidates ( Lactobacillus reuteri DM24MUS05, Lactobacillus plantarum DM23M20, and Lactobacillus rhamnosus MP108) that upregulated oligosaccharide‐synthesis genes. Probiotic consortium administration restored MO levels in DSS‐treated dams by mitigating enteric inflammation and reconstructing Lactobacillus ‐dominant microbiota. This study explores possible mechanisms linking gut microbiota dysbiosis to impaired MO biosynthesis. Our findings suggest that synergistic probiotics may represent a targeted intervention to counteract gut dysbiosis–associated impaired MO biosynthesis. These results position microbiota modulation as a promising, translatable approach for improving maternal‐infant health outcomes.

BackgroundGut microbiota contributes to human health. Little is known about the self-resilience of the gut microbiota after dysbiosis. This study aimed to investigate the self-resilience of the gut microbiome at different ages and the effects of diet on its recovery capacity in adulthood.MethodsA rodent model of antibiotic-induced dysbiosis was used. Microscopy was used to observe morphological changes in the mucosa. In addition, 16S rRNA sequencing and polymerase chain reaction-denaturing gradient gel electrophoresis were performed to identify the bacterial taxa and microbiome structure, respectively.ResultsThe diversity of the gut microbiota in infant mice was recovered by the sixth week, while relative abundance of Ruminococcaceae_UCG_014 was low and did not return to normal levels. Gut microbiota in young adult mice recovered in the fourth week. Prevotellaceae and Alloprevotella were significantly higher in the high-fat-diet group than those in the control group. The elderly mice had three, two, four, and seven statistically different genera between the dysbiosis and control groups at weeks 6, 8, 10, and 12, respectively. Intestinal epithelial structure and cecum index are restored with microbiota repaired.DiscussionThe gut microbiota in infant and adult mice is more capable of self- resilience, the composition of the microbiota and mucosal morphology of the intestine can be largely restored. Adding protein and fat to the diet accelerated colony recovery in young adult mice in the short term. In elderly mice, the resilience of the gut microbiota was reduced, and the occurrence of dysbiosis at this stage may accelerate organismal aging and affect the lifespan. A limitation of this study is that all data were derived from mice. Therefore, we must be cautious about translating the microbiome results from mice to humans.

Human milk oligosaccharides (HMOs) are vital milk carbohydrates that help promote the microbiota-dependent growth and immunity of infants. Sialic acid (SA) is a crucial component of sialylated milk oligosaccharides (S-MOs); however, the effects of SA supplementation in lactating mothers on S-MO biosynthesis and their breastfed infants are unknown. Probiotic intervention during pregnancy or lactation demonstrates promise for modulating the milk glycobiome. Here, we evaluated whether SA and a probiotic (Pro) mixture could increase S-MO synthesis in lactating mothers and promote the microbiota development of their breastfed neonates. The results showed that SA+Pro intervention modulated the gut microbiota and 6'-SL contents in milk of maternal rats more than the SA intervention, which promoted Lactobacillus reuteri colonization in neonates and immune development. Deficient 6'-SL in the maternal rat milk of St6gal1 knockouts (St6gal1-/-) disturbed intestinal microbial structures in their offspring, thereby impeding immune tolerance development. SA+Pro intervention in lactating St6gal1 +/- rats compromised the allergic responses of neonates by promoting 6 '-SL synthesis and the neonatal gut microbiota. Our findings from human mammary epithelial cells (MCF-10A) indicated that the GPR41-PI3K-Akt-PPAR pathway helped regulate 6 '-SL synthesis in mammary glands after SA+Pro intervention through the gut - breast axis. We further validated our findings using a human-cohort study, confirming that providing SA+Pro to lactating Chinese mothers increased S-MO contents in their breast milk and promoted gut Bifidobacterium spp. and Lactobacillus spp. colonization in infants, which may help enhance immune responses. Collectively, our findings may help alter the routine supplementation practices of lactating mothers to modulate milk HMOs and promote the development of early-life gut microbiota and immunity.

Hyperuricemia is a prevalent metabolic disorder that arises from abnormal purine metabolism and reduced excretion of uric acid (UA). The gut microbiota plays a significant role in the biosynthesis and excretion of UA. Probiotics capable of purine degradation possess the potential to prevent hyperuricemia. Our study aimed to screen probiotics in areas with abundant dairy products and longevity populations in China, which could attenuate the level of UA and explore the underlying mechanism. In this study, twenty-three lactic acid bacteria isolated from healthy Chinese infant feces and traditional fermented foods such as hurood and lump milk were evaluated for the ability to tolerance acid, bile, artificial gastric juice, and artificial intestinal juice to determine the potential of the candidate strains as probiotics. Eight strains were identified as possessing superior tolerance to simulated intestinal conditions and were further analyzed by high-performance liquid chromatography (HPLC), revealing that Limosilactobacillus reuteri HCS02-001 (Lact-1) and Lacticaseibacillus paracasei HCS17-040 (Lact-2) possess the most potent ability to degrade purine nucleosides. The effect of Lact-1 and Lact-2 on hyperuricemia was evaluated by intervening with them in the potassium oxonate and adenine-induced hyperuricemia Balb/c mice model in vivo. Our results showed that the level of serum UA in hyperuricemic mice can be efficiently reduced via the oral administration of Lact-1 (p < 0.05). It significantly inhibited the levels of liver inflammatory cytokines and hepatic xanthine oxidase through a TLR4/MyD88/NF-κB pathway across the gut–liver axis. Furthermore, UA transporters ABCG2 and SLC2A9 were substantially upregulated by the intervention of this probiotic. Fecal ATP levels were significantly induced, while fecal xanthine dehydrogenase and allantoinase levels were increased following probiotics. RNA sequencing of HT-29 cells line treated with Lact-1 and its metabolites demonstrated significant regulation of pathways related to hyperuricemia. In summary, these findings demonstrate that Limosilactobacillus reuteri HCS02-001 possesses a capacity to ameliorate hyperuricemia by inhibiting UA biosynthesis via enhancing gastrointestinal barrier functions and promoting UA removal through the upregulation of urate transporters, thereby providing a basis for the probiotic formulation by targeting the gut microbiota.

The aim of this study was to evaluate the effect of Lactobacillus delbrueckii subsp. lactis (L.del) on vaginal microbiota (VM) dysbiosis and vaginal radiation injury in gynecologic cancer patients. The inhibitory effects of L.del on cervical cancer cells were also studied in vitro. Gynecologic cancer patients receiving radiotherapy were randomized into control and L.del intervention groups. The control group received radiotherapy, while the intervention group received radiotherapy and L.del intervention (1 capsule/day placed into the deep vagina from the first day of radiotherapy until the end of treatment). Vaginal swab samples were collected on the first day pre-treatment and the last day post-treatment. DNA from 54 patients was extracted and assessed by the 16S rRNA sequencing method. Radiotherapy resulted in vaginal microbiome dysbiosis characterized by increased phylogenetic diversity and increased abundance of Brevundimonas, Streptococcus and Prevotella, but a decreased abundance of Lactobacillus. Level 2 vaginal radiation injury was positively associated with the abundance of Brevundimonas and gram-negative non-fermenting bacteria. Administration of L.del attenuated the reduction of Lactobacillus while also inhibiting the abundance of Streptococcus and Prevotella, thereby ameliorating radiotherapy-related vaginal microbiota dysbiosis. CLD inhibited the in vitro proliferation of SiHa cells by altering the expression of BCL2, HPV16-E6, HPV16-E7, IL6, MAP7, BAX, Caspase-3, Caspase-9 and LTF. In conclusion, L. del application can alleviate radiation-induced vaginal dysbiosis and restore Lactobacillus dominance of the vaginal microbiome. Moreover, CLD was found to inhibit cell growth and promote the apoptosis of SiHa cells in vitro. The registration number for this clinical trial is ChiCTR1900021784.

Objective To observe the clinical effect of coated probiotics on patients with functional constipation and the changes of gut microbiota. Methods Ten patients with functional constipation in Gastroenterology Department of Dalian Second People’s Hospital from January to March in 2022 were enrolled and treated with coated probiotics for 7 days. The changes of gut microbiota were detected before and after probiotics administration and 3 and 7 days after drug withdrawal by using 16S rDNA technology to evaluate whether the patients’ constipation symptom was improved. Results Both PAC-QOL and CSI score were significantly decreased after the treatment（all P＜0.01）, and fecal characters were improved. At 3 days and 7 days after withdrawal, Ace index and Chao1 index were higher than before（all P＜0.05）. After taking the drug, the relative abundances of Klebsiella, Lactococcus and Bacteroides increased, while those of Blautia and Anaerostipes decreased at genus level. At species level, the relative abundances of Lactobacillus plantarum, Klebsiella quasipneumoniae, Enterococcus faecium and Megasphaera elsdenii increased, while that of Anaerostipes hadrus decreased. Conclusion Coated probiotics can improve functional constipation, increase the relative abundance of intestinal microbiota in patients, and make gut microbiota structure more similar to that of healthy people.

Gut microbiota contributes to human health. Plenty of studies demonstrate that antibiotics can disrupt gut ecosystem leading to dysbiosis. Little is known about the microbial variation of appendix and its up/downstream intestine after antibiotic treatment. This study aimed to investigate the microbiome and mucosal morphology of jejunum, appendix, and colon of rats in health and dysbiosis. A rodent model of antibiotic-induced dysbiosis was employed. Microscopy was used to observe mucosal morphological changes. 16S rRNA sequencing was performed for identifying bacterial taxa and microbiome structure. The appendices of dysbiosis were found enlarged and inflated with loose contents. Microscopy revealed the impairment of intestinal epithelial cells. High-throughput sequencing showed the Operational Taxonomic Units changed from 361 ± 33, 634 ± 18, 639 ± 19 in the normal jejunum, appendix, colon to 748 ± 98, 230 ± 11, 253 ± 16 in the disordered segments, respectively. In dysbiosis, Bacteroidetes translocated inversely from the colon and appendix (0.26%, 0.23%) to the jejunum (13.87% ± 0.11%); the relative abundance of all intestinal Enterococcaceae increased, while Lactobacillaceae decreased. Several bacterial clusters were found correlated to the normal appendix, whereas nonspecific clusters correlated to the disordered appendix. In conclusion, species richness and evenness reduced in the disordered appendix and colon; similar microbiome patterns were shared between the appendix and colon regardless of dysbiosis; site-specific bacteria were missing in the disordered appendix. Appendix is likely a transit region involving in upper and lower intestinal microflora modulation. The limitation of this study is all the data were derived from rats. We must be cautious about translating the microbiome results from rats to humans.

高尿酸血症(hyperuricemia,HUA)是一种涉及肝、肾、肠等多个器官的代谢性疾病,因尿酸代谢异常而引起代谢障碍.尿酸在肝脏和肾脏中的代谢途径目前已经被阐明,但在肠道内的代谢途径尚未完全清晰.肠道菌群在人体肠道中定植,与宿主存在互惠共生的关系,在宿主的代谢和免疫调节中起着至关重要的作用.肠道菌群结构的变化可能引起代谢紊乱,肠道菌群参与嘌呤代谢酶的合成和炎症因子的释放,与HUA的发生发展密切相关.肠道菌群作为探讨HUA发病机制的切入点,已成为新的研究热点.本综述主要阐述HUA与肠道菌群之间的关系,探讨肠道菌群抗HUA的机制,如肠道菌群促进嘌呤和尿酸分解代谢,影响尿酸排泄,以及HUA引起的肠道炎症反应等,以期为通过调节肠道菌群来治疗HUA提供一定的依据.

Several studies have confirmed that the pathophysiological progression of Alzheimer’s disease (AD) is closely related to changes in the intestinal microbiota; thus, modifying the intestinal microbiota has emerged as a new way to treat AD. Effective interventions for gut microbiota include the application of probiotics and other measures such as fecal microbiota transplantation (FMT). However, the application of probiotics ignores that the intestine is a complete microecosystem with competition among microorganisms. FMT also has issues when applied to patient treatment. In a previous study, we found that eight species of bacteria that are isolated with high frequency in the normal intestinal microbiota (i.e., intestinal dominant microbiota) have biological activities consistent with the effects of FMT. In this article, we confirmed that the treatment of intestinal dominant microbiota significantly restored intestinal microbiota abundance and composition to normal levels in APP/PS1 mice; downregulated brain tissue pro-inflammatory cytokines (IL-1β and IL-6) and amyloid precursor protein (APP) and β-site APP cleavage enzyme 1 (BACE1) expression levels; and reduced the area of Aβ plaque deposition in the brain hippocampus. Our study provides a new therapeutic concept for the treatment of AD, adjusting the intestinal microecological balance through dominant intestinal microbiota may be an alternative to FMT.

The human gastrointestinal mucosa is colonized by thousands of microorganisms, which participate in a variety of physiological functions. Intestinal dysbiosis is closely associated with the pathogenesis of several human diseases. Innate lymphoid cells (ILCs), which include NK cells, ILC1s, ILC2s, ILC3s and LTi cells, are a type of innate immune cells. They are enriched in the mucosal tissues of the body, and have recently received extensive attention. The gut microbiota and its metabolites play important roles in various intestinal mucosal diseases, such as inflammatory bowel disease (IBD), allergic disease, and cancer. Therefore, studies on ILCs and their interaction with the gut microbiota have great clinical significance owing to their potential for identifying pharmacotherapy targets for multiple related diseases. This review expounds on the progress in research on ILCs differentiation and development, the biological functions of the intestinal microbiota, and its interaction with ILCs in disease conditions in order to provide novel ideas for disease treatment in the future.

Allergic respiratory disease is a worldwide and increasingly prevalent health problem. Many researchers have identified complex changes in the microbiota of the respiratory and intestinal tracts in patients with allergic respiratory diseases. These affect immune response and influence the progression of disease. However, the diversity of bacterial changes in such cases make it difficult to identify a specific microorganism to target for adjustment. Recent research evidence suggests that common bacterial variations present in allergic respiratory disease are associated with immune disorders. This finding could lead to the discovery of potential therapeutic targets in cases of allergic respiratory disease. In this review, we summarize current knowledge of bacteria changes in cases of allergic respiratory disease, to identify changes commonly associated with immune disorders, and thus provide a theoretical basis for targeting therapies of allergic respiratory disease through effective modulation of key bacteria.

Allergic respiratory disease is a worldwide health problem with increasing incidence and incurable properties. Extensive studies have found complex changes in the microbiota of the respiratory and intestinal tracts in allergic respiratory diseases, which affect the immune response and further influence the disease progression. The wide and diverse microbiota alterations in allergic respiratory disease make it difficult to find the exact microorganism to target for adjustment. Current evidence suggests that these common microbiota variations present in allergic respiratory disease are associated with immune disorders, which could be a potential therapeutic target for allergic respiratory disease. This review summarizes the current knowledge on microbiota changes in allergic respiratory disease, with the aim of identifying common microbiota changes associated with immune disorders and providing a theoretical basis for targeting therapies for allergic respiratory disease through effective modulation of key bacteria.