Agglutinins to anaerobic bacteria in crohn's disease and in indian patients with diarrhoea

Howells, B.; Matthews, N.; Mayberry, J F; Rhodes, J.

doi:10.1099/00222615-17-2-207

Cited by 11 publications

(1 citation statement)

References 8 publications

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“…From the results it is concluded that the agglutination reactions with the coccoid anaer-obes are a useful diagnostic aid for CD and for the differentiation between CD and UC. The occurrence of agglutinins to the coccoid anaerobes has been confirmed recently in an international study with 937 coded sera from seventeen centres all over the world (Wensinck et al, 1983) and in other studies (Auer et ak, 1983a, b;Howells et al, 1984).…”

Section: Bacterial Serum Antibodiesmentioning

confidence: 66%

The human faecal flora and Crohn’s disease

Merwe

1984

Antonie van Leeuwenhoek

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The aetiology of Crohn's disease (CD), a chronic inflammatory disease of the intestines, is not known but a genetic predisposition to CD has been well demonstrated. Studies on the isolation of bacteria from tissues and the faecal flora from CD patients are reviewed and their results compared with those from our laboratory. Serum antibodies against a variety of bacteria have been described but none has been found to be specific for CD. In our laboratory, higher numbers of coccoid anaerobes have been found in the faecal flora of CD patients. The use of agglutination reactions with four coccoid anaerobes as a diagnostic aid for CD is reviewed. No evidence has been found, however, for a primary role of the agglutinating antibodies in the pathogenesis of CD. On the other hand, one of the coccoid strains has been found to have several characteristics suggesting a role in CD, such as activation of the alternative pathway of complement, the failure of opsonization by specific IgG antibody and the binding of (non-specific) IgG onto the bacteria by the Fc portion. The composition of the faecal flora has been found to depend on genetic characteristics of the host. It is suggested that the genetic predisposition to CD is based on the genetically determined indigenous faecal flora present.

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Section: Bacterial Serum Antibodiesmentioning

confidence: 66%

The human faecal flora and Crohn’s disease

Merwe

1984

Antonie van Leeuwenhoek

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The B-Cell System in Inflammatory Bowel Disease

Brandtzæg

Carlsen

Halstensen

2006

Immune Mechanisms in Inflammatory Bowel Disease

120

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Secretory immunity is the best-defined part ot the mucosal immune system. This adaptive humoral defense mechanism depends on a fine-tuned cooperation between secretory epithelia and local plasma cells. Such mucosal immunocytes produce preferentially dimers and larger polymers of immunoglobulin A (collectively called pIgA), which contain J chain and therefore can bind to the epithelial secretory component (SC). This transmembrane glycoprotein functions as pIg receptor (pIgR) that also translocates pentameric IgM to the epithelial surface. B cells with a high level of J-chain expression and pIg-pIgR interactions at mucosal effector sites are thus necessary for the generation of secretory antibodies (SIgA and SIgM). Secretory antibodies perform immune exclusion in a first-line defense, thereby counteracting microbial colonization and mucosal penetration of soluble antigens. However, local production of pIgA is significantly down-regulated in inflammatory bowel disease (IBD), as revealed by strikingly decreased J-chain expression. Although the total increase of the immunocyte population in IBD lesions probably compensates for the relatively reduced pIgA production, decreased pIgR/SC expression in regenerating and dysplastic epithelium signifies that the SIgA system is topically deficient. There is, moreover, a significant shift from IgA2 to IgA1 production, the latter subclass being less resistant to proteolytic degradation. These changes--together with activation of mucosal macrophages and a dramatic increase of IgG-producing cells--may reflect local establishment of a second defense line which, however, is unsuccessful in its attempt to eliminate antigens derived from the indigenous microbial flora. Such a 'frustrated' local humoral immune system results in altered immunological homeostasis and jeopardized mucosal integrity. Complement activation observed in relation to epithelium-bound IgG1 in ulcerative colitis indicates, moreover, that the surface epithelium is subjected to immunological attack by an autoimmune reaction. These luminal deposits regularly contain terminal cytotoxic complement, and often also C3b as a sign of persistent activation. Comparison of identical twins, discordant with regard to ulcerative colitis, suggests that the markedly skewed local IgG1 response seen in this IBD entity may be genetically determined. The initial event(s) eliciting B-cell driven immunopathology in IBD remains unknown. Abrogation of oral tolerance to certain antigens from commensal bacteria has been suggested as a putative early mechanism, and lymphoid neogenesis and hyperplasia in the lesions most likely signify massive microbial overstimulation of the local B-cell system. Such ectopic lymphoid microcompartments may contribute substantially to the proinflammatory systemic-type of B-cell responses occurring in established IBD lesions.

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