Influence Of Microbiota Research Articles

The influence of gut microbiota on membranous nephropathy: A two-sample Mendelian randomization study.

Therapeutic approaches that target the gut microbiota may be helpful in the potential prevention and treatment of membranous nephropathy (MN). Several studies demonstrated a correlation between gut microbiota and MN. However, the confounding evidence cannot prove a causal relationship between gut microbiota and MN. The aim of our study is to assess genome-wide association study data for a causal relationship between gut microbiota and MN using a two-sample Mendelian randomization (MR) approach. Inverse variance weighted (IVW) was used as the primary technique to determine the association of genetic variants from gut microbiota and MN patients. Besides, sensitivity analyses confirmed the accuracy of the results. Finally, we applied false discovery rate (FDR) correction to results with IVW < 0.05 during multiple hypothesis testing. The results from IVW estimates indicated that Bacillales exhibited a significant association with MN, acting as a risk factor (OR = 1.52, 95% CI: 1.14 - 2.02, p = 0.005). In addition, our univariable MR results showed that 7 bacterial taxa (Melainabacteria, Butyricicoccus, Catenibacterium, Ruminiclostridium5, RuminococcaceaeUCG003, RuminococcaceaeUCG013, and Gastranaerophilales) had suggestive associations with MN. The sensitivity analysis did not reveal any significant heterogeneity in the instrumental variables or horizontal pleiotropy. Our findings provided causal evidence for the effect of gut microbiota on MN patients and broadened the spectrum of bacterial taxa that might be involved in the pathogenesis of MN. These selected bacterial taxa hold promise as new biomarkers, which may aid in designing targeted therapeutic modalities for MN, improving our comprehension of the gut-kidney axis.

Lung Microbiome in Lung Cancer: A New Horizon in Cancer Study.

Lung cancer is the second most prevalent cancer worldwide and a leading cause of cancer-related deaths. Recent technological advancements have revealed that the lung microbiome, previously thought to be sterile, is host to various microorganisms. The association between the lung microbiome and lung cancer initiation, progression, and metastasis is complex and contradictory. However, disruption in the homeostasis of microbiome compositions correlated with the increased risk of lung cancer. This review summarizes current knowledge about the most recent developments and trends in lung cancer-related microbiota or microbial components. This article aims to provide information on this rapidly evolving field while giving context to the general role of the lung microbiome in lung cancer. In addition, this review briefly discussed the causative association of lung microbiome with lung cancer. We will review the mechanisms by which lung microbiota influence carcinogenesis, focusing on microbiota dysbiosis. Moreover, we will also discuss the host-microbiome interaction as it plays a crucial role in stimulating and regulating the immune response. Finally, we will provide information on the diagnostic role of the microbiome in lung cancer. This article aims to offer an overview of the lung microbiome as a predictive and diagnostic biomarker in lung cancer.

Identification of patterns of microbiota influence on the pathogenetic mechanisms of systemic lupus erythematosus development

Systemic lupus erythematosus (SLE) is a complex, multifactorial autoimmune disease characterized by multisystem involvement. Although the pathogenesis of SLE is not fully understood, numerous studies have shown that the composition of the microbiota can influence the course of the disease. The microbiota plays a key role in the development of immune defense and is an integral part of immune homeostasis. Dysbiosis of the intestinal, oral and vaginal microbiota can have a significant impact on the development of inflammatory and autoimmune diseases. The review addresses recent studies on the microbiota, with a particular focus on changes in the composition of the gut microbiota and their impact on SLE. Data from several studies suggest that there is a link between SLE and certain patterns of dysbiosis.

Exploring the Role of the Gut Microbiota in Colorectal Cancer Development

Colorectal cancer is currently a public health concern due to its high incidence, morbidity, and mortality rates. Researchers have identified the intestinal microbiome as a crucial factor in the development of this disease. Currently, specialized literature data support the role of the microbiota in both the development of colorectal cancer and resistance to oncological therapies. Therefore, studying the composition of the gut microbiome can aid in creating risk assessment tools to identify specific populations that would benefit from tailored screening approaches. Also, manipulation of the intestinal microbiome can be useful in improving the response to chemotherapy or immunotherapy. Identifying the pathogenic mechanisms responsible for this causal link can aid in the discovery of novel treatment targets. This article will provide the latest information regarding the influence of the intestinal microbiota on the development and progression of colorectal cancer.

Identification of Causal Relationships between Gut Microbiota and Influenza a Virus Infection in Chinese by Mendelian Randomization.

Numerous studies have reported a correlation between gut microbiota and influenza A virus (IAV) infection and disease severity. However, the causal relationship between these factors remains inadequately explored. This investigation aimed to assess the influence of gut microbiota on susceptibility to human infection with H7N9 avian IAV and the severity of influenza A (H1N1)pdm09 infection. A two-sample Mendelian randomization analysis was conducted, integrating our in-house genome-wide association study (GWAS) on H7N9 susceptibility and H1N1pdm09 severity with a metagenomics GWAS dataset from a Chinese population. Twelve and fifteen gut microbiotas were causally associated with H7N9 susceptibility or H1N1pdm09 severity, separately. Notably, Clostridium hylemonae and Faecalibacterium prausnitzii were negative associated with H7N9 susceptibility and H1N1pdm09 severity, respectively. Moreover, Streptococcus peroris and Streptococcus sanguinis were associated with H7N9 susceptibility, while Streptococcus parasanguini and Streptococcus suis were correlated with H1N1pdm09 severity. These results provide novel insights into the interplay between gut microbiota and IAV pathogenesis as well as new clues for mechanism research regarding therapeutic interventions or IAV infections. Future studies should concentrate on clarifying the regulatory mechanisms of gut microbiota and developing efficacious approaches to reduce the incidence of IAV infections, which could improve strategy for preventing and treating IAV infection worldwide.

Towards a personalized prediction, prevention and therapy of insomnia: gut microbiota profile can discriminate between paradoxical and objective insomnia in post-menopausal women

BackgroundInsomnia persists as a prevalent sleep disorder among middle-aged and older adults, significantly impacting quality of life and increasing susceptibility to age-related diseases. It is classified into objective insomnia (O-IN) and paradoxical insomnia (P-IN), where subjective and objective sleep assessments diverge. Current treatment regimens for both patient groups yield unsatisfactory outcomes. Consequently, investigating the neurophysiological distinctions between P-IN and O-IN is imperative for devising novel precision interventions aligned with primary prediction, targeted prevention, and personalized medicine (PPPM) principles.Working hypothesis and methodology.Given the emerging influence of gut microbiota (GM) on sleep physiology via the gut-brain axis, our study focused on characterizing the GM profiles of a well-characterized cohort of 96 Italian postmenopausal women, comprising 54 insomniac patients (18 O-IN and 36 P-IN) and 42 controls, through 16S rRNA amplicon sequencing. Associations were explored with general and clinical history, sleep patterns, stress, hematobiochemical parameters, and nutritional patterns.ResultsDistinctive GM profiles were unveiled between O-IN and P-IN patients. O-IN patients exhibited prominence in the Coriobacteriaceae family, including Collinsella and Adlercreutzia, along with Erysipelotrichaceae, Clostridium, and Pediococcus. Conversely, P-IN patients were mainly discriminated by Bacteroides, Staphylococcus, Carnobacterium, Pseudomonas, and respective families, along with Odoribacter.ConclusionsThese findings provide valuable insights into the microbiota-mediated mechanism of O-IN versus P-IN onset. GM profiling may thus serve as a tailored stratification criterion, enabling the identification of women at risk for specific insomnia subtypes and facilitating the development of integrated microbiota-based predictive diagnostics, targeted prevention, and personalized therapies, ultimately enhancing clinical effectiveness.

Gut microbiota from B-cell-specific TLR9-deficient NOD mice promote IL-10+ Breg cells and protect against T1D.

Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of insulin-producing β cells. Toll-like receptor 9 (TLR9) plays a role in autoimmune diseases, and B cell-specific TLR9 deficiency delays T1D development. Gut microbiota are implicated in T1D, although the relationship is complex. However, the impact of B cell-specific deficiency of TLR9 on intestinal microbiota and the impact of altered intestinal microbiota on the development of T1D are unclear. This study investigated how gut microbiota and the intestinal barrier contribute to T1D development in B cell-specific TLR9-deficient NOD mice. Additionally, this study explored the role of microbiota in immune regulation and T1D onset. The study assessed gut permeability, gene expression related to gut barrier integrity, and gut microbiota composition. Antibiotics depleted gut microbiota, and fecal samples were transferred to germ-free mice. The study also examined IL-10 production, Breg cell differentiation, and their impact on T1D development. B cell-specific TLR9-deficient NOD mice exhibited increased gut permeability and downregulated gut barrier-related gene expression. Antibiotics restored gut permeability, suggesting microbiota influence. Altered microbiota were enriched in Lachnospiraceae, known for mucin degradation. Transferring this microbiota to germ-free mice increased gut permeability and promoted IL-10-expressing Breg cells. Rag-/- mice transplanted with fecal samples from Tlr9 fl/fl Cd19-Cre+ mice showed delayed diabetes onset, indicating microbiota's impact. B cell-specific TLR9 deficiency alters gut microbiota, increasing gut permeability and promoting IL-10-expressing Breg cells, which delay T1D. This study uncovers a link between TLR9, gut microbiota, and immune regulation in T1D, with implications for microbiota-targeted T1D therapies.

Microbiota influence on behavior: Integrative analysis of serotonin metabolism and behavioral profile in germ-free mice.

Previous studies on germ-free (GF) animals have described altered anxiety-like and social behaviors together with dysregulations in brain serotonin (5-HT) metabolism. Alterations in circulating 5-HT levels and gut 5-HT metabolism have also been reported in GF mice. In this study, we conducted an integrative analysis of various behaviors as well as markers of 5-HT metabolism in the brain and along the GI tract of GF male mice compared with conventional (CV) ones. We found a strong decrease in locomotor activity, accompanied by some signs of increased anxiety-like behavior in GF mice compared with CV mice. Brain gene expression analysis showed no differences in HTR1A and TPH2 genes. In the gut, we found decreased TPH1 expression in the colon of GF mice, while it was increased in the cecum. HTR1A expression was dramatically decreased in the colon, while HTR4 expression was increased both in the cecum and colon of GF mice compared with CV mice. Finally, SLC6A4 expression was increased in the ileum and colon of GF mice compared with CV mice. Our results add to the evidence that the microbiota is involved in regulation of behavior, although heterogeneity among studies suggests a strong impact of genetic and environmental factors on this microbiota-mediated regulation. While no impact of GF status on brain 5-HT was observed, substantial differences in gut 5-HT metabolism were noted, with tissue-dependent results indicating a varying role of microbiota along the GI tract.

Effects of immune cells in mediating the relationship between gut microbiota and myelodysplastic syndrome: a bidirectional two-sample, two-step Mendelian randomization study

BackgroundThe definitive establishment of a causal relationship between gut microbiota and myelodysplastic syndrome (MDS) has not been achieved. Furthermore, the involvement of immune cells in mediating the connection between gut microbiota and MDS is presently unclear.MethodsTo elucidate the bidirectional correlation between gut microbiota and MDS, as well as to investigate the mediating role of immune cells, a bidirectional two-sample, two-step Mendelian randomization (MR) study was conducted. Summary statistics were obtained from genome-wide association studies (GWAS), including MDS (456,348 individuals), gut microbiota (18,340 individuals), and 731 immune cells signatures (3757 individuals).ResultsGenetically predicted eight gut microbiota traits were significantly associated with MDS risk, but not vice versa. Through biological annotation of host-microbiome shared genes, we found that immune regulation may mediate the impact of gut microbiota on MDS. Subsequently, twenty-three immunophenotypes that exhibited significant associations with MDS risk and five of these immunophenotypes were under the causal influence of gut microbiota. Importantly, the causal effects of gut microbiota on MDS were significantly mediated by five immunophenotypes, including CD4 +T cell %leukocyte, CD127 on CD45RA − CD4 not regulatory T cell, CD45 on CD33 + HLA DR + WHR, CD33 on basophil, and Monocyte AC.ConclusionsGut microbiota was causally associated with MDS risk, and five specific immunophenotypes served as potential causal mediators of the effect of gut microbiota on MDS. Understanding the causality among gut microbiota, immune cells and MDS is critical in identifying potential targets for diagnosis and treatment.

The investigation of the role of oral-originated Prevotella-induced inflammation in childhood asthma.

The oral and gut microbiota play significant roles in childhood asthma pathogenesis. However, the communication dynamics and pathogenic mechanisms by which oral microbiota influence gut microbiota and disease development remain incompletely understood. This study investigated potential mechanisms by which oral-originated gut microbiota, specifically Prevotella genus, may contribute to childhood asthma etiology. Oral swab and fecal samples from 30 asthmatic children and 30 healthy controls were collected. Microbiome composition was characterized using 16S rRNA gene sequencing and metagenomics. Genetic distances identified potential oral-originated bacteria in asthmatic children. Functional validation assessed pro-inflammatory properties of in silico predicted microbial mimicry peptides from enriched asthma-associated species. Fecal metabolome profiling combined with metagenomic correlations explored links between gut microbiota and metabolism. HBE cells treated with Prevotella bivia culture supernatant were analyzed for lipid pathway impacts using UPLC-MS/MS. Children with asthma exhibited distinct oral and gut microbiota structures. Prevotella bivia, P. disiens, P. oris and Bacteroides fragilis were enriched orally and intestinally in asthmatics, while Streptococcus thermophilus decreased. P. bivia, P. disiens and P. oris in asthmatic gut likely originated orally. Microbial peptides induced inflammatory cytokines from immune cells. Aberrant lipid pathways characterized asthmatic children. P. bivia increased pro-inflammatory and decreased anti-inflammatory lipid metabolites in HBE cells. This study provides evidence of Prevotella transfer from oral to gut microbiota in childhood asthma. Prevotella's microbial mimicry peptides and effects on lipid metabolism contribute to disease pathogenesis by eliciting immune responses. Findings offer mechanistic insights into oral-gut connections in childhood asthma etiology.

Multifunctional role of oral bacteria in the progression of non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of liver disorders of varying severity, ultimately leading to fibrosis. This spectrum primarily consists of NAFL and non-alcoholic steatohepatitis. The pathogenesis of NAFLD is closely associated with disturbances in the gut microbiota and impairment of the intestinal barrier. Non-gut commensal flora, particularly bacteria, play a pivotal role in the progression of NAFLD. Notably, Porphyromonas gingivalis, a principal bacterium involved in periodontitis, is known to facilitate lipid accumulation, augment immune responses, and induce insulin resistance, thereby exacerbating fibrosis in cases of periodontitis-associated NAFLD. The influence of oral microbiota on NAFLD via the "oral-gut-liver" axis is gaining recognition, offering a novel perspective for NAFLD management through microbial imbalance correction. This review endeavors to encapsulate the intricate roles of oral bacteria in NAFLD and explore underlying mechanisms, emphasizing microbial control strategies as a viable therapeutic avenue for NAFLD.

The impact of depression-mediated gut microbiota composition on Irritable Bowel Syndrome: A Mendelian study

ObjectiveThis study uses a two-sample Mendelian randomization (MR) analysis to delineate the causal influence of gut microbiota on the occurrence of irritable bowel syndrome (IBS), concurrently assessing the potential mediating function of depression within this framework. MethodsSeveral two-sample MR methods were used to assess the causal repercussions of gut microbiota on the onset of both IBS and depression. Following this, gut microbiota and depression, which demonstrated notable causal associations, were integrated as exposure variables in a multivariable Mendelian randomization (MVMR) framework to construct a model encompassing gut microbiota, depression, and IBS. Mediation effects were assessed by examining the indirect pathway of gut microbiota → depression → IBS. ResultsTwo-sample MR analysis unveiled a statistically significant causal association (P < 0.05) between specific bacterial group within the gut microbiota, notably p_Actinobacteria(OR = 0.829225), c_Clostridia(OR = 0.798897), s_Desulfovibrio_piger(OR = 1.163912), g_Streptococcus(OR = 1.132735), c_Actinobacteria(OR = 0.829224), and the onset of IBS. In the MVMR analysis, the relationship between depression and IBS was significant across Model 3, Model 7, Model 8, and Model 13 (P < 0.05). Assessment of mediation effects revealed that c_Clostridia and o_Clostridiales indirectly impacted IBS through depression, with masking effect ratios of 168.46 % and 168.44 %, respectively. ConclusionThese findings underscore a resilient causal association between the composition of gut microbiota and the initiation of IBS. Furthermore, depression serves as a mediator for particular groups of gut bacteria, thereby contributing to the development of IBS. These observations imply that interventions targeting mental health may potentially alleviate the risk of IBS onset attributable to adverse configurations of gut microbiota.

#1270 Exploring the shift in gut microbiota due to renal ischemia/reperfusion injury in rats

Abstract Background and Aims Acute kidney injury (AKI) due to renal ischemia/reperfusion (I/R) is a major clinical problem in renal transplantation and partial nephrectomy, which is associated with morbidity and mortality and substantial healthcare expenditures, but there is no effective and specific treatment. Recently, the clinical impact of the interaction between gut bacteria and the kidney function has become increasingly clear. Experimental evidence has highlighted a bidirectional relationship between gut microbiota and kidney disease. Therefore, we investigated the possibility that I/R can ameliorate AKI by studying gut-renal interactions and gut microbiota in AKI. Method We induced varying degrees of renal I/R injury in adult male Wistar rats by clamping the left renal pelvis for 30 and 45 minutes, simulating mild and severe conditions, respectively. These samples were subjected to extensive histologic examination using standard techniques such as hematoxylin and eosin (HE), Sirius Red, and F4/80 staining. In addition, we performed a quantitative analysis of the mRNA expression levels of fibrotic and inflammatory markers in both kidney and colon tissues using real-time PCR. Gut microbiota genomic DNA was extracted from rat feces and microbial 16S ribosomal RNA (rRNA) gene sequencing was performed. Results Renal function deteriorated with increasing ischemia time and fibrosis progressed, as confirmed by Sirius Red staining and qPCR of fibrosis genes such as TGFB. The expression of inflammatory genes such as IL-1B and IL-6 was also increased. The expression of inflammatory genes such as Toll-like receptor, C3, and IL-1B in the intestine also increased with ischemia time. In the fecal microbiota, the total read percentage of Bacteroides acidifaciens at the species level increased with increasing ischemia time. Conclusion The observed shifts in gut microbiota composition may serve as a critical indicator of chronic kidney disease (CKD)-induced gut dysbiosis secondary to AKI. This finding highlights the need for further research into the identification and migration patterns of the gut microbiota, which represents a promising avenue for early detection, prevention, and therapeutic intervention in AKI. Future investigations elucidating the mechanisms by which the microbiota influence IRI-induced AKI and the development of practical therapeutic strategies have the potential to significantly improve clinical outcomes in patients suffering from IRI-induced AKI.

ADVANCEMENTS IN UNDERSTANDING THE MOLECULAR MECHANISMS REGULATING URIC ACID METABOLISM IN THE INTESTINE

This review provides contemporary insights into the direct and indirect pathogenetic connections between purine compound metabolism and biochemical processes within the cells of the gastrointestinal system. A thorough analysis of recent publications from 2000 to 2024, sourced from databases including Scopus, PubMed, eLIIBRARY, and Google Scholar, was conducted. Uric acid serves as the end product of purine-containing compound catabolism. Its concentration is intricately regulated through the collaboration of the kidneys and gastrointestinal organs, namely the small intestine and liver. Gout, a chronic condition, emerges from the interplay between molecular genetic factors and external influences. Elevated levels of urates in the blood serum (hyperuricemia) and the deposition of sodium urate crystals in organs and tissues set off a cascade of inflammatory and fibrotic processes within mucosal, smooth muscle, parenchymal, and endothelial cells, including those within the gastrointestinal tract. Normally, a person excretes about 1.5 g of uric acid per day. Under physiological conditions, two-thirds of uric acid is excreted from the body by the kidneys, one-third through the intestines, and a small part is excreted with bile. The hypothesis that links the pathogenesis of hyperuricemia with “renal overload” suggests that the disease may develop as a result of impaired renal excretion with insufficient elimination of uric acid through the intestines. Part of uric acid transport systems actively works in hepatocytes and enterocytes, which determines its formation and clearance. Uric acid transporter proteins are divided into two categories: urate reabsorption transporters and urate excretion transporters, their expression is regulated by transcription factors, hormones and metabolites of intestinal microflora. The influence of intestinal microbiota on uric acid metabolism is related to its participation in purine metabolism, decomposition and elimination of uric acid with metabolites of intestinal flora and inhibition of gouty inflammation and is evaluated as a new therapeutic potential in gout and hyperuricemia, which allows to avoid kidney damage and urolithiasis.

Comprehensive analysis of the gut microbiota in patients with chronic obstructive pulmonary disease of varying severity-A prospective, observational study

Accumulating evidence has highlighted the influence of the gut microbiota on lung immunity. We examined the effects of changes in intestinal microecology on the development of Chronic Obstructive Pulmonary Disease (COPD) and identified microbial biomarkers for acute exacerbations of COPD (AECOPD). Fecal samples were collected from 30 patients with stable COPD, 30 patients with AECOPD, and 10 healthy individuals. Fecal microbiological profiles were analyzed using 16S rRNA gene sequencing. The results showed a distinct difference in the bacterial community composition between the AECOPD, COPD, and healthy control groups. The COPD and AECOPD groups had higher levels of Firmicutes but lower levels of Bacteroidetes compared to the healthy control group at the phylum level. At the genus level, there was an increased abundance of Lachnoclostridium, Alistipes, Streptococcus, and Prevotella in COPD and AECOPD patients. Increasing levels of Lachnoclostridium and Prevotella may indicate an acute exacerbation of COPD. This study identified specific microbial biomarkers associated with AECOPD and characterized the composition of gut microbiota in patients with AECOPD.

Three stepwise pH progressions in stratum corneum for homeostatic maintenance of the skin

The stratum corneum is the outermost skin layer with a vital role in skin barrier function. It is comprised of dead keratinocytes (corneocytes) and is known to maintain its thickness by shedding cells, although, the precise mechanisms that safeguard stratum corneum maturation and homeostasis remain unclear. Previous ex vivo studies have suggested a neutral-to-acidic pH gradient in the stratum corneum. Here, we use intravital pH imaging at single-corneocyte resolution to demonstrate that corneocytes actually undergo differentiation to develop three distinct zones in the stratum corneum, each with a distinct pH value. We identified a moderately acidic lower, an acidic middle, and a pH-neutral upper layer in the stratum corneum, with tight junctions playing a key role in their development. The upper pH neutral zone can adjust its pH according to the external environment and has a neutral pH under steady-state conditions owing to the influence of skin microbiota. The middle acidic pH zone provides a defensive barrier against pathogens. With mathematical modeling, we demonstrate the controlled protease activation of kallikrein-related peptidases on the stratum corneum surface that results in proper corneocyte shedding in desquamation. This work adds crucial information to our understanding of how stratum corneum homeostasis is maintained.

Influence of epigenetics and microbiota in early‑life development: A possible role for exosomes (Review)

Influence of epigenetics and microbiota in early‑life development: A possible role for exosomes (Review)

Insulin therapy for elderly patients with type 2 diabetes mellitus

The prevalence of type 2 diabetes among older people is increasing every year. The main pathogenetic mechanisms of type 2 diabetes in elderly patients include disruption of the intestinal microbiota, cellular aging, oxidative stress and mitochondrial dysfunction, immune and inflammatory processes. Short-chain fatty acids produced by the intestinal microbiota influence inflammatory processes in pancreatic β-cells. Cellular senescence causes the secretion of different cytokines, chemokines, growth factors and proteases, exacerbating the proinflammatory state and increasing insulin resistance of the tissues. Oxidative stress and mitochondrial dysfunction decrease the ATP synthesis process and increase the formation of reactive oxygen species. Changes in the immune system in elderly patients contribute to autoimmune processes and systemic inflammation. Clinical features of diabetes mellitus in old age include asymptomatic progression, impaired recognition of hypoglycemia, impaired cognitive function, and muscle atrophy. The progressive decline in β-cells function in type 2 diabetes requires insulin therapy in many patients. Biphasic insulins allow to control both basal and postprandial glycemia, are easy to use and are indicated for patients who have difficulty counting amount of carbohydrates. However, it is worth remembering a balanced approach to prescribing and deintensifying therapy.

Intestinal microbiota and gallstone disease – is there a connection?

Cholelithiasis is a fairly common disease of the digestive system, affecting from 10 % to 15 % of the adult population. Despite many studies devoted to this problem, the mechanisms of formation of gallstone disease have not been fully elucidated. Recently, aspects of the influence of the intestinal microbiota on the mechanisms of formation of various pathologies of the gastrointestinal tract such as non-alcoholic fatty liver disease, inflammatory bowel diseases, irritable bowel syndrome, pancreatic diseases, gastroesophageal reflux disease have been considered. The presented review article examines the possible involvement of the gastrointestinal microbiome in the pathogenesis of gallstone disease. The article discusses the role of microorganisms and their metabolites in the formation of gallstones.

Critical COVID-19, Victivallaceae abundance, and celiac disease: A mediation Mendelian randomization study.

Celiac disease exhibits a higher prevalence among patients with coronavirus disease 2019. However, the potential influence of COVID-19 on celiac disease remains uncertain. Considering the significant association between gut microbiota alterations, COVID-19 and celiac disease, the two-step Mendelian randomization method was employed to investigate the genetic causality between COVID-19 and celiac disease, with gut microbiota as the potential mediators. We employed the genome-wide association study to select genetic instrumental variables associated with the exposure. Subsequently, these variables were utilized to evaluate the impact of COVID-19 on the risk of celiac disease and its potential influence on gut microbiota. Employing a two-step Mendelian randomization approach enabled the examination of potential causal relationships, encompassing: 1) the effects of COVID-19 infection, hospitalized COVID-19 and critical COVID-19 on the risk of celiac disease; 2) the influence of gut microbiota on celiac disease; and 3) the mediating impact of the gut microbiota between COVID-19 and the risk of celiac disease. Our findings revealed a significant association between critical COVID-19 and an elevated risk of celiac disease (inverse variance weighted [IVW]: P = 0.035). Furthermore, we observed an inverse correlation between critical COVID-19 and the abundance of Victivallaceae (IVW: P = 0.045). Notably, an increased Victivallaceae abundance exhibits a protective effect against the risk of celiac disease (IVW: P = 0.016). In conclusion, our analysis provides genetic evidence supporting the causal connection between critical COVID-19 and lower Victivallaceae abundance, thereby increasing the risk of celiac disease.