Adherent-invasive Escherichia coli isolated from Crohn's disease patients induce granulomas in vitro

Meconi, Sonia; Vercellone, Alain; Levillain, Florence; Payré, Bruno; Saati, Talal Al; Capilla, Florence; Desreumaux, Pierre; Darfeuille‐Michaud, Arlette; Altare, Frédéric

doi:10.1111/j.1462-5822.2006.00868.x

Cited by 113 publications

(74 citation statements)

References 51 publications

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“…A possible role for AIEC in the etiopathogenesis of CD in susceptible hosts is summarized in Figure 1. The sequential steps involved in the induction of disease by the bacteria are: (1) abnormal colonization via binding to the CEACAM6 receptor, which is overexpressed in the ileal mucosa of CD patients [13] ; (2) ability to adhere to and to invade intestinal epithelial cells, which allows bacteria to cross the mucosal barrier [37] ; (3) survival and replication within infected macrophages in the lamina propria; and (4) induction of TNF-α secretion [45] and granuloma formation [58] . AIEC strains could colonize the ileal mucosa of CD patients by binding to CEACAM6, translocate across the human intestinal barrier to move into deep tissues, and once there, continuously activate immune cells.…”

Section: Resultsmentioning

confidence: 99%

“…Using an in vitro model of human granuloma [57] , CD-associated AIEC LF82 were reported to induce aggregation of infected macrophages, some of which fused to form multinucleated giant cells and subsequent recruitment of lymphocytes. Analysis of the cell aggregates indicated that they are very similar to the early stages of epithelioid granulomas [58] .…”

Section: Granuloma Formationmentioning

confidence: 95%

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Role of bacteria in the etiopathogenesis of inflammatory bowel disease

Barnich

Darfeuille‐Michaud²

2007

WJG

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Increased numbers of mucosa-associated Escherichia coli are observed in both of the major inflammatory bowel diseases, Crohn's disease (CD) and ulcerative colitis (UC). A potential pathophysiological link between the presence of pathogenic invasive bacteria and genetic host susceptibility of patients with ileal CD is suspected. In CD patients, with increased ileal expression of the CEACAM6 molecule acting as a receptor recognized by type 1 pilus bacterial adhesin, and with the identification of mutations in the NOD2-encoding gene, the presence of pathogenic invasive bacteria could be the link between abnormal ileal bacterial colonization and innate immune responses to invasive bacteria. In a susceptible host, the sequential etiological steps of the disease induced by adherent-invasive E. coli (AIEC) are: (1) abnormal colonization via binding to the CEACAM6 receptor, which is overexpressed in the ileal mucosa of CD patients; (2) ability to adhere to and to invade intestinal epithelial cells, which allows bacteria to cross the mucosal barrier; (3) survival and replication within infected macrophages in the lamina propria; and (4) induction of tumor necrosis factor-α secretion and granuloma formation.

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Section: Resultsmentioning

confidence: 99%

Section: Granuloma Formationmentioning

confidence: 95%

Role of bacteria in the etiopathogenesis of inflammatory bowel disease

Barnich

Darfeuille‐Michaud²

2007

WJG

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“…23 This probably results in the formation of granulomas, as observed with the in vitro model of human granulomas, in which AIEC LF82 induces aggregation of infected macrophages, and sometimes their fusion to form multinucleated giant cells, and subsequent recruitment of lymphocytes. 26 Secretion of TNF-a by infected monocytes/macrophages is a common feature of pathogenic bacteria, but impaired macrophage TNF-a secretion has been reported following infection with some of them such as Brucella spp., meningitidis-associated E. coli K1, and Francisella tularensis. [27][28][29] In addition, TNF-a can have opposite effects on intracellular bacteria replication.…”

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confidence: 99%

Replication of Crohn's disease-associated AIEC within macrophages is dependent on TNF-α secretion

Bringer

Billard

Glasser

et al. 2012

Laboratory Investigation

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Adherent and invasive Escherichia coli (AIEC) associated with Crohn's disease are able to survive and to replicate extensively in active phagolysosomes within macrophages. AIEC-infected macrophages release large amounts of tumour necrosis factor-alpha (TNF-a) and do not undergo cell death. The aim of the present study was to determine what benefit AIEC bacteria could gain from inducing the release of large amounts of TNF-a by infected macrophages and to what extent the neutralization of TNF-a could affect AIEC intramacrophagic replication. Our results showed that the amount of TNF-a released by infected macrophages is correlated with the load of intramacrophagic AIEC bacteria and their intracellular replication. TNF-a secretion was not related to the number of bacteria entering host cells because when the number of bacteria internalized in macrophage was decreased by blocking lipid raft-dependent and clathrin-coated pits-dependent endocytosis, the amount of TNF-a secreted by infected macrophages was not modified. Interestingly, dose-dependent increases in the number of intracellular AIEC LF82 bacteria were observed when infected macrophages were stimulated with exogenous TNF-a, and neutralization of TNF-a secreted by AIEC-infected macrophages using anti-TNF-a antibodies induced a significant decrease in the number of intramacrophagic bacteria. These results indicate that AIEC bacteria use TNF-a as a Trojan horse to ensure their intracellular replication because replication of AIEC bacteria within macrophages induces the release of TNF-a, which in turn increases the intramacrophagic replication of AIEC. Neutralizing TNF-a secreted by infected macrophages may represent an effective strategy to control AIEC intracellular replication.

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“…By expressing long polar fimbriae, the bacteria interact with mouse and human Peyer's patches and translocate across microfold cells monolayers (83). AIEC are also able to survive and replicate extensively within a large, phagolysosome-like vacuole in macrophages (84) and AIEC-infected macrophages aggregate and fuse to form multinucleated giant cells in vitro (85).…”

Section: Gut Microbiotamentioning

confidence: 99%

Crohn’s Disease: a Role of Gut Microbiota and Nod2 Gene Polymorphisms in Disease Pathogenesis

Hrncírová

Krejsek

Šplı́chal

et al. 2014

Acta Med. (Hradec Kralove, Czech Repub.)

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Crohn’s disease is a chronic immune-mediated intestinal inflammation targeted against a yet incompletely defined subset of commensal gut microbiota and occurs on the background of a genetic predisposition under the influence of environmental factors. Genome-wide association studies have identified about 70 genetic risk loci associated with Crohn’s disease. The greatest risk for Crohn’s disease represent polymorphisms affecting the CARD15 gene encoding nucleotide-binding oligomerization domain 2 (NOD2) which is an intracellular sensor for muramyl dipeptide, a peptidoglycan constituent of bacterial cell wall. The accumulated evidence suggests that gut microbiota represent an essential, perhaps a central factor in the induction and maintaining of Crohn’s disease where dysregulation of normal co-evolved homeostatic relationships between intestinal microbiota and host mucosal immune system leads to intestinal inflammation. Taken together, these findings identify Crohn’s disease as a syndrome of overlapping phenotypes that involves variable influences of genetic and environmental factors. A deeper understanding of different genetic abnormalities underlying Crohn’s disease together with the identification of beneficial and harmful components of gut microbiota and their interactions are essential conditions for the categorization of Crohn’s disease patients, which enable us to design more effective, preferably causative, individually tailored therapy.

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Adherent-invasive Escherichia coli isolated from Crohn's disease patients induce granulomas in vitro

Cited by 113 publications

References 51 publications

Role of bacteria in the etiopathogenesis of inflammatory bowel disease

Role of bacteria in the etiopathogenesis of inflammatory bowel disease

Replication of Crohn's disease-associated AIEC within macrophages is dependent on TNF-α secretion

Crohn’s Disease: a Role of Gut Microbiota and Nod2 Gene Polymorphisms in Disease Pathogenesis

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