GipA Factor Supports Colonization of Peyerʼs Patches by Crohnʼs Disease-associated Escherichia Coli

Vazeille, Emilie; Chassaing, Benoît; Buisson, Anthony; Dubois, A.; Vallée, Amélie de; Billard, Elisabeth; Neut, Christel; Bommelaer, Gilles; Colombel, Jean–Frédéric; Barnich, Nicolas; Darfeuille‐Michaud, Arlette; Bringer, Marie-Agnès

doi:10.1097/mib.0000000000000609

Cited by 41 publications

(40 citation statements)

References 67 publications

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“…We conducted presence/absence and phylogenetic analyses on the following LF82-associated genes: rpoE ;39 htrA (also known as degP and ptd );40 dsbA, 41 hfq, 42 and AIEC/IBD-associated E. coli genes : pduC 29 (propanediol utilisation), fyuA, ibeA, K1, kpsmTII, 17 vgrG , hcp , vasD , vasG , impL , impK (type VI secretion system genes), and vat , insA , insB, 30 fimH, 28 afaC 45 and clb (pks island),46and the combination of gipA and lpfA, 43 or lpfA alone 44 45. Nine of the 41 strains harboured the afaC gene (H504, H305, H020, H296, 61–1 ti1, 52–2 ti10, 52–1 ti3, 18–4 ti12, 18–3 ti5), 4 of which were AIEC (36% of all AIEC strains), belonged to ST95 and had an O18:H7 serotype.…”

Section: Resultsmentioning

confidence: 99%

Comparative genomics of Crohn's disease-associated adherent-invasiveEscherichia coli

O’Brien

Bringer

Holt

et al. 2016

Gut

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Section: Resultsmentioning

confidence: 99%

Comparative genomics of Crohn's disease-associated adherent-invasiveEscherichia coli

O’Brien

Bringer

Holt

et al. 2016

Gut

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“…GipA expression is induced by certain intracellular, GI (bile salts) and phagolysosomal (ROS and acid pH) conditions. Deletion of gipA dampens the proinflammatory response and AIEC replication inside macrophages 53. AIEC killing by macrophages could be inhibited by microbial mannan in a TLR4 and MyD88-dependent manner 132…”

Section: Aiec and The Gut Immune Systemmentioning

confidence: 99%

Adherent-invasive Escherichia coli in inflammatory bowel disease

Palmela

Chevarin

et al. 2017

Gut

Self Cite

405

318

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Intestinal microbiome dysbiosis has been consistently described in patients with IBD. In the last decades, Escherichia coli, and the adherent-invasive E coli (AIEC) pathotype in particular, has been implicated in the pathogenesis of IBD. Since the discovery of AIEC, two decades ago, progress has been made in unravelling these bacteria characteristics and its interaction with the gut immune system. The mechanisms of adhesion of AIEC to intestinal epithelial cells (via FimH and cell adhesion molecule 6) and its ability to escape autophagy when inside macrophages are reviewed here. We also explore the existing data on the prevalence of AIEC in patients with Crohn’s disease and UC, and the association between the presence of AIEC and disease location, activity and postoperative recurrence. Finally, we highlight potential therapeutic strategies targeting AIEC colonisation of gut mucosa, including the use of phage therapy, bacteriocins and antiadhesive molecules. These strategies may open new avenues for the prevention and treatment of IBD in the future.

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“…[137][138][139] Adherence and invasion of pathobionts usually requires expression of specific genes such as proteases in E. faecalis and GipA (growth in Peyer' s patches) in AIEC. [140][141][142][143] In addition to attachment and invasion, pathobiont species also impair normal IEC functions for intestinal homeostasis. C. concisus, a gram-negative microbe that is increased in pediatric and adult IBD patients, inhibits expression of the tight junction-associated proteins ZO-1 and occludin, as well as their association with tight junction complexes leading to a less regulated intestinal barrier.…”

Section: Alterations Of Intestinal Epithelial Integritymentioning

confidence: 99%

Epithelial-microbial diplomacy: escalating border tensions drive inflammation in inflammatory bowel disease

King

McCole

2019

Intest Res

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Inflammatory bowel diseases (IBD) are chronic conditions of the gastrointestinal tract-the main site of host-microbial interaction in the body. Development of IBD is not due to a single event but rather is a multifactorial process where a patient’s genetic background, behavioral habits, and environmental exposures contribute to disease pathogenesis. IBD patients exhibit alterations to gut bacterial populations “dysbiosis” due to the inflammatory microenvironment, however whether this alteration of the gut microbiota precedes inflammation has not been confirmed. Emerging evidence has highlighted the important role of gut microbes in developing measured immune responses and modulating other host responses such as metabolism. Much of the work on the gut microbiota has been correlative and there is an increasing need to understand the intimate relationship between host and microbe. In this review, we highlight how commensal and pathogenic bacteria interact with host intestinal epithelial cells and explore how altered microenvironments impact these connections.

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GipA Factor Supports Colonization of Peyerʼs Patches by Crohnʼs Disease-associated Escherichia Coli

Abstract: GipA is required for optimal colonization of mouse PPs and survival within macrophages by AIEC, suggesting that this factor plays a role in AIEC promotion of Crohn's disease. Detection of gipA and lpfA could be a predictor for the presence of AIEC.

Cited by 41 publications

References 67 publications

Comparative genomics of Crohn's disease-associated adherent-invasiveEscherichia coli

Comparative genomics of Crohn's disease-associated adherent-invasiveEscherichia coli

Adherent-invasive Escherichia coli in inflammatory bowel disease

Epithelial-microbial diplomacy: escalating border tensions drive inflammation in inflammatory bowel disease

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