CD83+CCR7− Dendritic Cells Accumulate in the Subepithelial Dome and Internalize Translocated Escherichia coli HB101 in the Peyer's Patches of Ileal Crohn's Disease

Salim, Saad Y.; Silva, Manuel A.; Keita, Åsa V.; Larsson, Marie; Andersson, Peter; Magnusson, Karl‐Eric; Perdue, Mary H.; Söderholm, Johan D.

doi:10.2353/ajpath.2009.080273

Cited by 41 publications

(39 citation statements)

References 49 publications

(48 reference statements)

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“…A correlation exists between peak of CD case frequency (between 15 and 25 years old) and peak representing the number of PPs according to age, suggesting that CD develops as an inflammatory process specifically targeting these important lymphoid structures (36). Moreover, recent studies reported a defect in the intestinal barrier to control bacterial translocation across PPs of CD (37,38). It is well documented that several enteroinvasive pathogens, such as Yersinia, Shigella, and Salmonella, invade the intestinal mucosa via the M cells of the FAE (24,27,31).…”

Section: Discussionmentioning

confidence: 99%

Crohn disease–associated adherent-invasive E. coli bacteria target mouse and human Peyer’s patches via long polar fimbriae

Chassaing¹,

Rolhion²,

Vallée³

et al. 2011

J. Clin. Invest.

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219

203

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Crohn disease (CD) is a multifactorial disease in which an abnormal immune response in the gastrointestinal (GI) tract leads to chronic inflammation. The small intestine, particularly the ileum, of patients with CD is colonized by adherent-invasive E. coli (AIEC) -a pathogenic group of E. coli able to adhere to and invade intestinal epithelial cells. As the earliest inflammatory lesions are microscopic erosions of the epithelium lining the Peyer's patches (PPs), we investigated the ability of AIEC bacteria to interact with PPs and the virulence factors involved. We found that AIEC bacteria could interact with mouse and human PPs via long polar fimbriae (LPF). An LPF-negative AIEC mutant was highly impaired in its ability to interact with mouse and human PPs and to translocate across monolayers of M cells, specialized epithelial cells at the surface of PPs. The prevalence of AIEC strains harboring the lpf operon was markedly higher in CD patients compared with controls. In addition, increased numbers of AIEC, but not LPF-deficient AIEC, bacteria were found interacting with PPs from Nod2 -/-mice compared with WT mice. In conclusion, we have identified LPF as a key factor for AIEC to target PPs. This could be the missing link between AIEC colonization and the presence of early lesions in the PPs of CD patients.

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Section: Discussionmentioning

confidence: 99%

Crohn disease–associated adherent-invasive E. coli bacteria target mouse and human Peyer’s patches via long polar fimbriae

Chassaing¹,

Rolhion²,

Vallée³

et al. 2011

J. Clin. Invest.

Self Cite

219

203

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“…75 Consistently, abnormal development of Peyer's patches as well as increased permeability and bacterial translocation were observed in NOD2 deficient mice. 76 The findings that increased E. coli translocation occurs in follicle-associated epithelium or in Peyer's patches isolated from CD patients compared with non-IBD patients 77,78 and that increased numbers of Peyer's patches are found in CD, represent novel insights into CD pathophysiology by a previously unrecognized defect of intestinal barrier function in ileal CD.…”

Section: Listeria Monocytogenes Bacteroides Vulgatus Bacteroides Burgmentioning

confidence: 99%

Immunopathogenesis of inflammatory bowel disease

Matricon¹,

Barnich²,

Ardid³

2010

Self/Nonself

190

137

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REVIEW Definition and EpidemiologyInflammatory bowel disease (IBD) is characterized by severe inflammation of the small bowel and/or the colon leading to recurrent diarrhea and abdominal pain. Crohn disease (CD) and ulcerative colitis (UC) are the two main clinicopathological subtypes of IBD. Despite both being chronic and relapsing inflammatory diseases of the bowel, they can be differentiated by the location of the inflammation in the gastrointestinal tract and by Inflammatory bowel disease (IBD) is a group of idiopathic, chronic and relapsing inflammatory conditions of the gastrointestinal tract. Familial and epidemiological studies have stressed the involvement of genetic factors and have also shown the critical role of environmental factors such as sanitation and hygiene in the development of IBD. However, the molecular mechanisms of intestinal inflammation in IBD have long remained unknown. In recent years, the study of susceptibility genes involved in the detection of bacterial components and in the regulation of the host immune response has shed light onto the potential role of intestinal pathogens and gut flora in IBD immunobiology. This review presents current knowledge on intestinal epithelial barrier alterations and on dysfunction of mucosal innate and acquired immune responses in IBD. The data support the etiological hypothesis which argues that pathogenic intestinal bacteria and/or infectious agents initiate and perpetuate the inflammation of the gut through disruption of tolerance towards the commensal microbiota in an individual with genetic vulnerability. Immunopathogenesis of inflammatory bowel disease

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“…Indeed, causes underlying this disease are likely multifactorial. In general, studies have shown an increase in both DC and macrophage populations in the intestinal lamina propria in Crohn's Disease patients [20,32,33,[50][51][52]. Studies have also consistently shown that DCs in Crohn's Disease are more activated and have higher expression of microbial recognition receptors, particularly TLR4 [8,27,50,53,54].…”

Section: Phagocyte Subsets In the Intestine Of Patients With Crohn's mentioning

confidence: 92%

Intestinal dendritic cell and macrophage subsets: Tipping the balance to Crohn's Disease?

Magnusson

Wick

2011

European Journal of Microbiology and Immunology

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CD83+CCR7− Dendritic Cells Accumulate in the Subepithelial Dome and Internalize Translocated Escherichia coli HB101 in the Peyer's Patches of Ileal Crohn's Disease

Cited by 41 publications

References 49 publications

Crohn disease–associated adherent-invasive E. coli bacteria target mouse and human Peyer’s patches via long polar fimbriae

Crohn disease–associated adherent-invasive E. coli bacteria target mouse and human Peyer’s patches via long polar fimbriae

Immunopathogenesis of inflammatory bowel disease

Intestinal dendritic cell and macrophage subsets: Tipping the balance to Crohn's Disease?

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