Adherent-invasive Escherichia coli in inflammatory bowel disease

Rolhion, Nathalie; Darfeuille‐Michaud, Arlette

doi:10.1002/ibd.20176

Cited by 225 publications

(172 citation statements)

References 82 publications

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“…Adherent-invasive Escherichia coli has been isolated from ileal biopsy samples from patients with Crohn's disease. Pathogenic adherent-invasive Escherichia coli can colonize the ileal mucosa by adhering to intestinal epithelial cells, and is also a true invasive pathogen that is able to invade intestinal epithelial cells [22]. Adherent-invasive Escherichia coli also replicates in macrophages and stimulates production of tumor necrosis factor (TNF)-a by macrophages [22].…”

Section: Gut Microbiota and Ibdmentioning

confidence: 99%

“…Pathogenic adherent-invasive Escherichia coli can colonize the ileal mucosa by adhering to intestinal epithelial cells, and is also a true invasive pathogen that is able to invade intestinal epithelial cells [22]. Adherent-invasive Escherichia coli also replicates in macrophages and stimulates production of tumor necrosis factor (TNF)-a by macrophages [22]. In ulcerative colitis patients, Fusobacterium varium attaches to inflamed mucosa and invades ulcerated mucosa [23].…”

Section: Gut Microbiota and Ibdmentioning

confidence: 99%

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A breakthrough in probiotics: Clostridium butyricum regulates gut homeostasis and anti-inflammatory response in inflammatory bowel disease

2015

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Intestinal immune homeostasis is regulated by gut microbiota, including beneficial and pathogenic microorganisms. Imbalance in gut bacterial constituents provokes host proinflammatory responses causing diseases such as inflammatory bowel disease (IBD). The development of next-generation sequencing technology allows the identification of microbiota alterations in IBD. Several studies have shown reduced diversity in the gut microbiota of patients with IBD. Advances in gnotobiotic technology have made possible analysis of the role of specific bacterial strains in immune cells in the intestine. Using these techniques, we have shown that Clostridium butyricum as a probiotic induces interleukin-10-producing macrophages in inflamed mucosa via the Toll-like receptor 2/myeloid differentiation primary response gene 88 pathway to prevent acute experimental colitis. In this review, we focus on the new approaches for the role of specific bacterial strains in immunological responses, as well as the potential of bacterial therapy for IBD treatments.

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Section: Gut Microbiota and Ibdmentioning

confidence: 99%

Section: Gut Microbiota and Ibdmentioning

confidence: 99%

A breakthrough in probiotics: Clostridium butyricum regulates gut homeostasis and anti-inflammatory response in inflammatory bowel disease

2015

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“…However the relatively rapid, and recent, increase in the incidence of CD also points to a significant role for environmental factors in the aetiology of this disease. In recent years, a group of Escherichia coli called adherent-invasive Escherichia coli (AIEC) have been found to be present in the guts of CD patients at a higher frequency than in healthy subjects, leading to the suggestion that AIEC may be involved in initiating and/or maintaining the inflammation associated with CD (Negroni et al, 2012;Rhodes, 2007;Rolhion & Darfeuille-Michaud, 2007). AIEC have also been found associated with CD-like diseases in other mammals, e.g.…”

Section: Introductionmentioning

confidence: 99%

Glycolysis and pyrimidine biosynthesis are required for replication of adherent–invasive Escherichia coli in macrophages

et al. 2016

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Adherent-invasive Escherichia coli (AIEC) have been implicated in the aetiology of Crohn's disease (CD), a chronic inflammatory bowel condition. It has been proposed that AIEC-infected macrophages produce high levels of pro-inflammatory cytokines thus contributing to the inflammation observed in CD. AIEC can replicate in macrophages and we wanted to determine if bacterial replication was linked to the high level of cytokine production associated with AIECinfected macrophages. Therefore, we undertook a genetic analysis of the metabolic requirements for AIEC replication in the macrophage and we show that AIEC replication in this niche is dependent on bacterial glycolysis. In addition, our analyses indicate that AIEC have access to a wide range of nutrients in the macrophage, although the levels of purines and pyrimidines do appear to be limiting. Finally, we show that the macrophage response to AIEC infection is indistinguishable from the response to the non-replicating glycolysis mutant (DpfkAB) and a nonpathogenic strain of E. coli, MG1655. Therefore, AIEC does not appear to subvert the normal macrophage response to E. coli during infection.

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“…E. coli strains isolated from patients with active IBD frequently display pathogenic properties, such as adhesion to and invasion of host cells (6). A role for adherent-invasive E. coli (AIEC) in the pathogenesis of IBD, particularly in CD (7,8), has been supported by whole metagenome sequencing data from human cohort samples (9).…”

mentioning

confidence: 99%

QseC inhibition as an antivirulence approach for colitis-associated bacteria

Rooks

Veiga

Reeves

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Hosts and their microbes have established a sophisticated communication system over many millennia. Within mammalian hosts, this dynamic cross-talk is essential for maintaining intestinal homeostasis. In a genetically susceptible host, dysbiosis of the gut microbiome and dysregulated immune responses are central to the development of inflammatory bowel disease (IBD). Previous surveys of stool from the T-bet −/− Rag2 −/− IBD mouse model revealed microbial features that discriminate between health and disease states. Enterobacteriaceae expansion and increased gene abundances for benzoate degradation, two-component systems, and bacterial motility proteins pointed to the potential involvement of a catecholamine-mediated bacterial signaling axis in colitis pathogenesis. Enterobacteriaceae sense and respond to microbiota-generated signals and host-derived catecholamines through the two-component quorum-sensing Escherichia coli regulators B and C (QseBC) system. On signal detection, QseC activates a cascade to induce virulence gene expression. Although a single pathogen has not been identified as a causative agent in IBD, adherent-invasive Escherichia coli (AIEC) have been implicated. Flagellar expression is necessary for the IBD-associated AIEC strain LF82 to establish colonization. Thus, we hypothesized that qseC inactivation could reduce LF82's virulence, and found that an absence of qseC leads to down-regulated flagellar expression and motility in vitro and reduced colonization in vivo. We extend these findings on the potential of QseC-based IBD therapeutics to three preclinical IBD models, wherein we observe that QseC blockade can effectively modulate colitogenic microbiotas to reduce intestinal inflammation. Collectively, our data support a role for QseC-mediated bacterial signaling in IBD pathogenesis and indicate that QseC inhibition may be a useful microbiota-targeted approach for disease management.colitis | Escherichia coli | QseC | antivirulence | gut microbiome

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Adherent-invasive Escherichia coli in inflammatory bowel disease

Cited by 225 publications

References 82 publications

A breakthrough in probiotics: Clostridium butyricum regulates gut homeostasis and anti-inflammatory response in inflammatory bowel disease

A breakthrough in probiotics: Clostridium butyricum regulates gut homeostasis and anti-inflammatory response in inflammatory bowel disease

Glycolysis and pyrimidine biosynthesis are required for replication of adherent–invasive Escherichia coli in macrophages

QseC inhibition as an antivirulence approach for colitis-associated bacteria

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