T cell specificity and cross reactivity towards enterobacteria,<i>Bacteroides</i>,<i>Bifidobacterium</i>, and antigens from resident intestinal flora in humans

Duchmann, Rainer; May, Ekkehard; Heike, Michael; Knolle, Percy A.; Neurath, Markus F.; Büschenfelde, K H Meyer zum

doi:10.1136/gut.44.6.812

Cited by 254 publications

(157 citation statements)

References 46 publications

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“…It must be realized that bacterial products derived from the normal gut flora are capable of stimulating the T-cell activity [2] and proinflammatory cytokines [33±35]. CWs of closely related bacterial species have been found to differ in their ability of cytokine stimulation (Zhang et al, unpublished observations).…”

Section: Discussionmentioning

confidence: 99%

Experimental Chronic Arthritis and Granulomatous Inflammation Induced byBifidobacteriumCell Walls

et al. 2001

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Effects of cell walls (CWs) from two almost identical strains of Bifidobacterium adolescentis were studied in rats, using three different doses. A single i.p. injection of both CWs triggered a long‐lasting arthritis with CW degradation products present in the joint tissue. Histologically, the arthritis was characterized by inflammatory cells, synovial hyperplasia, pannus formation and bone erosion, closely resembling human rheumatoid arthritis (RA). In addition, CWs of the other strain induced a remarkable granuloma formation in the spleen and liver. Both CWs have the same peptidoglycan (PG) type A4α/β, but differ from each other in three aspects. CW of the granuloma inducing strain: firstly has more lysine and less ornithine in PG stem peptides; secondly is more resistant to lysozyme degradation, and thirdly is better retained in the spleen. All these in comparison to the other strain used. Such characteristics are associated with the capacity to induce chronic arthritis, but it remains open how crucial they are for the granuloma formation.

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Section: Discussionmentioning

confidence: 99%

Experimental Chronic Arthritis and Granulomatous Inflammation Induced byBifidobacteriumCell Walls

et al. 2001

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“…81 Similar to colitic mice, human IBD patients show enhanced immune responsiveness to gut bacterial antigens and concurrent loss of tolerance. 82,83 Some of the specific bacterial antigens driving disease in mouse models of colitis and human IBD have recently been identified. One key antigen that drives disease is flagellin, the major structural subunit of bacterial flagella (reviewed in ref.…”

Section: Role For Bacterial Antigens In Ibdmentioning

confidence: 99%

The role of T‐regulatory cells and Toll‐like receptors in the pathogenesis of human inflammatory bowel disease

Himmel¹,

Hardenberg²,

Piccirillo³

et al. 2008

Immunology

132

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SummaryTwo related chronic inflammatory diseases, Crohn's disease and ulcerative colitis, are together often referred to as inflammatory bowel disease (IBD). Current treatment options are not curative, and patients face lifelong therapy and debilitation. IBD is thought to be the product of a combination of genetic and environmental factors that result in the abnormal regulation of immune responses. Experimental models have demonstrated that normal CD4 + T-regulatory (Treg) cell responses and commensal bacteria are required for the maintenance of gut immune homeostasis. Recent evidence that CD4 + T cells express Toll-like receptors (TLRs) and respond directly to TLR ligands, suggests that signals from commensal bacteria may directly affect T-cell responses in the gut. In this review, we focus on evidence that defects in Treg cells may underlie IBD in humans. In addition, we discuss evidence that direct signaling via TLRs to T cells can affect IBD and that T-cell-dependent responses to bacterial proteins, such as flagellin, are central to the aetiology of this disease.

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“…In addition, the intestinal mucosa of CD patients is covered by adherent strains of Escherichia coli and other bacteria from the lumen, whereas these bacteria are absent from the normal small bowel mucosa (16,18,19). Furthermore, a loss in immunological tolerance toward luminal microbiota is observed in patients with CD (17). Thus, IBD pathogenesis likely results from a breach in effective mucosal barrier functions to constituents of the commensal microbiota (24).…”

mentioning

confidence: 99%

“…In addition to genetic factors in IBD, numerous studies have implicated a key role of the intestinal microbiota in disease pathogenesis, both in patients with IBD (15)(16)(17)(18)(19)(20) and in rodent models of IBD (for reviews, see refs. 21 and 22).…”

mentioning

confidence: 99%

Reduced Paneth cell α-defensins in ileal Crohn's disease

Wehkamp

Salzman

Porter

et al. 2005

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

911

809

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The pathogenesis of Crohn s disease (CD), an idiopathic inflammatory bowel disease, is attributed, in part, to intestinal bacteria that may initiate and perpetuate mucosal inflammation in genetically susceptible individuals. Paneth cells (PC) are the major source of antimicrobial peptides in the small intestine, including human ␣-defensins HD5 and HD6. We tested the hypothesis that reduced expression of PC ␣-defensins compromises mucosal host defenses and predisposes patients to CD of the ileum. We report that patients with CD of the ileum have reduced antibacterial activity in their intestinal mucosal extracts. These specimens also showed decreased expression of PC ␣-defensins, whereas the expression of eight other PC products either remained unchanged or increased when compared with controls. The specific decrease of ␣-defensins was independent of the degree of inflammation in the specimens and was not observed in either CD of the colon, ulcerative colitis, or pouchitis. The functional consequence of ␣-defensin expression levels was examined by using a transgenic mouse model, where we found changes in HD5 expression levels, comparable to those observed in CD, had a pronounced impact on the luminal microbiota. Thus, the specific deficiency of PC defensins that characterizes ileal CD may compromise innate immune defenses of the ileal mucosa and initiate and͞or perpetuate this disease.innate immunity ͉ intestine ͉ bacteria ͉ inflammatory bowel disease

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T cell specificity and cross reactivity towards enterobacteria,Bacteroides,Bifidobacterium, and antigens from resident intestinal flora in humans

Cited by 254 publications

References 46 publications

Experimental Chronic Arthritis and Granulomatous Inflammation Induced byBifidobacteriumCell Walls

Experimental Chronic Arthritis and Granulomatous Inflammation Induced byBifidobacteriumCell Walls

The role of T‐regulatory cells and Toll‐like receptors in the pathogenesis of human inflammatory bowel disease

Reduced Paneth cell α-defensins in ileal Crohn's disease

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