ChiA: a major player in the virulence of Crohn's disease-associated adherent and invasive (AIEC).

We investigated the role of ChiA and its associated polymorphisms in the interaction between Crohn's disease (CD)-associated adherent-invasive (AIEC) and intestinal mucosa. We observed a higher abundance of among the metagenome of CD patients compared to healthy subjects. In dextran sulfate sodium-induced colitis mice model, AIEC-LF82∆ colonization was reduced in ileal, colonic and fecal samples compared to wild-type LF82.

Increased levels of anti-Encephalitozoon intestinalis antibodies in patients with colorectal cancer.

Background: The prevalence of microsporidiosis in the general population, or within specific groups of individuals/patients, is largely underestimated. The absence of specific seroprevalence tools limits knowledge of the epidemiology of these opportunistic pathogens, although known since the 1980s. Since microsporidia hijack the machinery of its host cell and certain species multiply within intestinal cells, a potential link between the parasite and colorectal cancer (CRC) has been suggested.

AIEC-dependent pathogenic Th17 cell transdifferentiation in Crohn's disease is suppressed by and deletion.

Mucosal enrichment of the Adherent-Invasive (AIEC) pathotype and the expansion of pathogenic IFNγ-producing Th17 (pTh17) cells have been linked to Crohn's Disease (CD) pathogenesis. However, the molecular pathways underlying the AIEC-dependent pTh17 cell transdifferentiation in CD patients remain elusive. To this aim, we created and functionally screened a transposon AIEC mutant library of 10.

Preclinical and clinical evidence of the association of colibactin-producing with anxiety and depression in colon cancer.

Background: The association between the intestinal microbiota and psychiatric disorders is becoming increasingly apparent. The gut microbiota contributes to colorectal carcinogenesis (CRC), as demonstrated with colibactin-producing (CoPEC).

Aim: To evaluate the association between CoPEC prevalence and anxiety- and depressive-like behaviors with both preclinical and clinical approaches.

ATG16L1 in myeloid cells limits colorectal tumor growth in mice infected with colibactin-producing via decreasing inflammasome activation.

strains producing the genotoxin colibactin, designated as CoPEC (colibactin-producing ), have emerged as an important player in the etiology of colorectal cancer (CRC). Here, we investigated the role of macroautophagy/autophagy in myeloid cells, an important component of the tumor microenvironment, in the tumorigenesis of a susceptible mouse model infected with CoPEC. For that, a preclinical mouse model of CRC, the mice, with deficiency specifically in myeloid cells (/) and the corresponding control mice (), were infected with a clinical CoPEC strain 11G5 or its isogenic mutant 11G5 that does not produce colibactin.

Identification of autophagy receptors for the Crohn's disease-associated adherent-invasive .

Introduction: Crohn's disease (CD) is a chronic inflammatory bowel disease, of which the etiology involves genetic, environmental and microbial factors. Adherent-invasive (AIEC) and polymorphisms in autophagy-related genes have been implicated in CD etiology. Autophagy is a key process for the maintenance of cellular homeostasis, which allows the degradation of damaged cytoplasmic components and pathogens via lysosome.

Colibactin-producing enhance resistance to chemotherapeutic drugs by promoting epithelial to mesenchymal transition and cancer stem cell emergence.

Human colorectal cancers (CRCs) are readily colonized by colibactin-producing (CoPEC). CoPEC induces DNA double-strand breaks, DNA mutations, genomic instability, and cellular senescence. Infected cells produce a senescence-associated secretory phenotype (SASP), which is involved in the increase in tumorigenesis observed in CRC mouse models infected with CoPEC.

Effects of a Cycling versus Running HIIT Program on Fat Mass Loss and Gut Microbiota Composition in Men with Overweight/Obesity.

Purpose: High-intensity interval training (HIIT) can efficiently decrease total and (intra-)abdominal fat mass (FM); however, the effects of running versus cycling HIIT programs on FM reduction have not been compared yet. In addition, the link between HIIT-induced FM reduction and gut microbiota must be better investigated. The aim of this study was to compare the effects of two 12-wk HIIT isoenergetic programs (cycling vs running) on body composition and fecal microbiota composition in nondieting men with overweight or obesity.

Perinatal foodborne titanium dioxide exposure-mediated dysbiosis predisposes mice to develop colitis through life.

Background: Perinatal exposure to titanium dioxide (TiO), as a foodborne particle, may influence the intestinal barrier function and the susceptibility to develop inflammatory bowel disease (IBD) later in life. Here, we investigate the impact of perinatal foodborne TiO exposure on the intestinal mucosal function and the susceptibility to develop IBD-associated colitis. Pregnant and lactating mother mice were exposed to TiO until pups weaning and the gut microbiota and intestinal barrier function of their offspring was assessed at day 30 post-birth (weaning) and at adult age (50 days).

Host-microbiota relationship in the pathophysiology of aseptic abscess syndrome: protocol for a multicentre case-control study (ABSCESSBIOT).

Introduction: Aseptic abscess (AA) syndrome is a rare disease whose pathophysiology is unknown. It is often associated with inflammatory bowel disease and characterised by sterile inflammation with collections of neutrophils affecting several organs, especially the spleen. Microbiota are known to influence local and systemic immune responses, and both gut and oral microbiota perturbations have been reported in diseases associated with AA syndrome.

Cytotoxic necrotizing factor 1 hinders colon tumorigenesis induced by colibactin-producing in mice.

Colorectal cancer (CRC) patients are frequently colonized by colibactin-producing (CoPEC) (>40%), which enhances tumorigenesis in mouse models of CRC. We observed that 50% of CoPEC also contains the gene, which encodes cytotoxic necrotizing factor-1 (CNF1), an enhancer of the eukaryotic cell cycle. The impact of its co-occurrence with colibactin (Clb) has not yet been investigated.

Microbiome and Behçet's disease: a systematic review.

The aim of this review was to describe the changes in the microbiota of patients with Behçet's disease (BD) and the mechanisms involved in the relationship between the microbiome and immunity in BD. A systematic search for relevant articles was made on PubMed and the Cochrane Library database using the following terms: "microbiota AND Behçet's disease" or "microbiome AND Behçet's disease". Sixteen articles were included in a qualitative synthesis.

Genes mcr improve the intestinal fitness of pathogenic E. coli and balance their lifestyle to commensalism.

Background: The plasmid-mediated resistance gene mcr-1 confers colistin resistance in Escherichia coli and paves the way for the evolution to pan-drug resistance. We investigated the impact of mcr-1 in gut colonization in the absence of antibiotics using isogenic E. coli strains transformed with a plasmid encoding or devoid of mcr-1.

Epigenetic master regulators HDAC1 and HDAC5 control pathobiont Enterobacteria colonization in ileal mucosa of Crohn's disease patients.

AIEC Adherent-Invasive ; BSA Bovine serum albumin; CD Crohn's disease; CEABAC10 Carcinoembryonic antigen bacterial artificial chromosome 10; CEACAM Carcinoembryonic antigen-related cell adhesion molecule; FBS Fetal bovine serum; IBD Inflammatory Bowel Disease; HAT Histone acetyltransferase; HDAC Histone deacetylase; kDa KiloDalton; SAHA Suberoylanilide Hydroxamic Acid; Scr Scramble.

An adherent-invasive Escherichia coli-colonized mouse model to evaluate microbiota-targeting strategies in Crohn's disease.

Adherent-invasive Escherichia coli (AIEC) were investigated for their involvement in the induction/chronicity of intestinal inflammation in Crohn's disease (CD). AIEC gut establishment is favoured by overexpression of the glycoprotein CEACAM6 in the ileal epithelium. We generated a transgenic mouse model, named 'Vill-hCC6', in which the human CEACAM6 gene was under the control of the villin promoter, conditioning expression in the small intestine.

Specific Localization and Quantification of the Oligo-Mouse-Microbiota (OMM ) by Fluorescence In Situ Hybridization (FISH).

The oligo-mouse-microbiota (OMM ) is a widely used syncom that colonizes gnotobiotic mice in a stable manner. It provides several fundamental functions to its murine host, including colonization resistance against enteric pathogens. Here, we designed and validated specific fluorescence in situ hybridization (FISH) probes to detect and quantify OMM strains on intestinal tissue cross sections.

Identification of Virulence Markers and Phylogenetic Groups' Association, and Antimicrobial Susceptibility of Uropathogenic Isolates.

Background: Urinary tract infections represent a world public health problem, which is caused mainly by Uropathogenic Escherichia coli. Although they are originally found in the intestinal microbiota in the majority of the cases, urinary tract infections can also be caused by intra-intestinal pathogenic E. coli.

Mucolytic bacteria license pathobionts to acquire host-derived nutrients during dietary nutrient restriction.

Pathobionts employ unique metabolic adaptation mechanisms to maximize their growth in disease conditions. Adherent-invasive Escherichia coli (AIEC), a pathobiont enriched in the gut mucosa of patients with inflammatory bowel disease (IBD), utilizes diet-derived L-serine to adapt to the inflamed gut. Therefore, the restriction of dietary L-serine starves AIEC and limits its fitness advantage.