IgG Antibodies Against Common Gut Bacteria Are More Diagnostic for Crohn's Disease Than IgG Against Mannan or Flagellin

Adams, Rachel J.; Heazlewood, Sharise P.; Gilshenan, Kristen; O’Brien, M. Margaret; McGuckin, Michael A.; Florin, Timothy H.

doi:10.1111/j.1572-0241.2007.01577.x

Cited by 48 publications

(48 citation statements)

References 51 publications

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“…[116][117][118] In addition, overactivation of B cells in IBD results in a high production of mucosal IgG auto-antibodies directed against commensal bacterial antigens from the intestinal lumen. [118][119][120] These data suggest a shift from antibodies of the protector subtype (IgA) to the aggressive subtype (IgG) leading to mucosal inflammation.…”

mentioning

confidence: 89%

Immunopathogenesis of inflammatory bowel disease

Matricon¹,

Barnich²,

Ardid³

2010

Self/Nonself

193

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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mentioning

confidence: 89%

Immunopathogenesis of inflammatory bowel disease

Matricon¹,

Barnich²,

Ardid³

2010

Self/Nonself

193

137

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“…As previously stated, current knowledge about the interaction between extracellular proteins and the GALT mainly derives from data involving commensal bacterial groups. In this context, it has been observed that some proteins secreted by the commensal microbiota might be responsible for the anomalous immune response observed in the framework of inflammatory bowel disease (Adams et al, 2008;Ivison & Steiner, 2008;Schoepfer et al, 2008).…”

Section: Proteins Secreted By Probiotic Bacteriamentioning

confidence: 99%

“…In this context, the existence of antibodies directed against certain proteins secreted by the commensal microbiota in the framework of certain autoimmune diseases is known. Some examples of these proteins are porin OmpC from Escherichia coli, porin OmpW from Bacteroides caccae, protein I2 from Pseudomonas fluorescens and flagellin from Clostridium coccoides (Adams et al, 2008;Furrie et al, 2004;Iltanen et al, 2006;Müller et al, 2008). Theoretically, it is possible that certain extracellular proteins secreted by probiotic bacteria might also reach the gut mucosa, acting as molecular effectors responsible for downstream responses in mucosal cells.…”

Section: Proteins Secreted By Probiotic Bacteriamentioning

confidence: 99%

Extracellular proteins secreted by probiotic bacteria as mediators of effects that promote mucosa–bacteria interactions

2010

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During the last few years, a substantial body of scientific evidence has accumulated suggesting that certain surface-associated and extracellular components produced by probiotic bacteria could be responsible for some of their mechanisms of action. These bacterial components would be able to directly interact with the host mucosal cells; they include exopolysaccharides, bacteriocins, lipoteichoic acids and surface-associated and extracellular proteins. Extracellular proteins include proteins that are actively transported to the bacterial surroundings through the cytoplasmic membrane, as well as those that are simply shed from the bacterial surface. Compared to the other bacterial components, the interactive ability of extracellular proteins/ peptides has been less extensively studied. In this review, current findings supporting an interaction between extracellular proteins/peptides produced by probiotic bacteria (strains of the genera Bifidobacterium, Lactobacillus and Escherichia) and host mucosal cells are discussed. Research needs and future trends are also considered.

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“…Previous reports 13,14 suggested that bacterial flagellin might play a role in the pathogenesis of mucosal idio- pathic inflammation such as IBD. To elucidate the immune pathogenic role of flagellin-specific immune response in the intestinal inflammation, colonic biopsy samples were collected from 23 Crohn's disease patients; 6 "normal" samples were collected from surgical removed tissue from patients with colonic cancer to use as controls (the marginal normal tissue was used in this study).…”

Section: Colocalization Of Flagellin/flagellin-specific Igg/ Fc␥ri Onmentioning

confidence: 99%

“…12 Specific antibodies against flagellin, which are at low levels or under detectable levels in healthy subjects, have been de-tected in the serum of IBD patients. 13,14 Anti-flagellin IgG has the potential to activate immune cells such as dendritic cells, macrophages and mast cells via binding the Fc␥ receptors (Fc␥R) on the surface of the cells. Mastocytosis is one of the pathological features of IBD.…”

mentioning

confidence: 99%

Fc Gamma Receptor Signaling in Mast Cells Links Microbial Stimulation to Mucosal Immune Inflammation in the Intestine

Chen

Feng

Zheng

et al. 2008

The American Journal of Pathology

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Microbes and microbial products are closely associated with the pathogenesis of inflammatory bowel disease (IBD); however, the mechanisms behind this connection remain unclear. It has been previously reported that flagellin-specific antibodies are increased in IBD patient sera. As mastocytosis is one of the pathological features of IBD, we hypothesized that flagellin-specific immune responses might activate mast cells that then contribute to the initiation and maintenance of intestinal inflammation. Thirtytwo colonic biopsy samples were collected from IBD patients. A flagellin/flagellin-specific IgG/Fc gamma receptor I complex was identified on biopsied mast cells using both immunohistochemistry and co-immunoprecipitation experiments; this complex was shown to co-localize on the surfaces of mast cells in the colonic mucosa of patients with IBD. In addition, an ex vivo study showed flagellin-IgG was able to bind to human mast cells. These cells were found to be sensitized to flagellin-specific IgG; re-exposure to

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IgG Antibodies Against Common Gut Bacteria Are More Diagnostic for Crohn's Disease Than IgG Against Mannan or Flagellin

Cited by 48 publications

References 51 publications

Immunopathogenesis of inflammatory bowel disease

Immunopathogenesis of inflammatory bowel disease

Extracellular proteins secreted by probiotic bacteria as mediators of effects that promote mucosa–bacteria interactions

Fc Gamma Receptor Signaling in Mast Cells Links Microbial Stimulation to Mucosal Immune Inflammation in the Intestine

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