T-cellular immune reactions (in macrophage inhibition factor assay) against Mycobacterium paratuberculosis, Mycobacterium kansasii, Mycobacterium tuberculosis, Mycobacterium avium in patients with chronic inflammatory bowel disease
Article Abstract:
Crohn's disease, or regional ileitis, is an inflammatory condition of the intestine characterized by diarrhea, abdominal pain, anemia, weight loss, and symptoms of bowel obstruction. The cause of Crohn's disease is not known, but it has been suggested that infestation with mycobacteria (the type of bacterial parasite which causes tuberculosis and leprosy) may be a causal factor. Johne's disease, a similar condition in cattle, is known to be caused by infection with Mycobacterium paratuberculosis. To evaluate the possibility that an inappropriate immune response (either exaggerated or suppressed) to M. paratuberculosis, or to a similar bacterial parasite, might be involved in Crohn's disease, a study was performed involving 35 patients with Crohn's disease, 28 patients with ulcerative colitis (a similar inflammatory condition affecting the colon, which is not thought to result from bacterial infection), and 25 healthy control subjects. Subjects were injected with inactivated M. paratuberculosis, Mycobacterium kansasii, Mycobacterium tuberculosis, and Mycobacterium avium; the response of the immune system was evaluated. There were no differences in the percentages of patients in the three groups showing various types of responses to each of the bacterial antigens. This suggests that an altered response to one of these bacteria is not responsible for Crohn's disease. In addition, many of the control subjects showed mycobacterial activation of the immune system (indicating prior or current infestation), suggesting that individuals can be exposed to these bacteria with no adverse effects. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Gut
Subject: Health
ISSN: 0017-5749
Year: 1990
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Role of the CS1 adhesion motif of fibronectin in T cell adhesion to synovial membrane and peripheral lymph node endothelium
Article Abstract:
The very late antigen-4-vascular cell adhesion molecule-1 (VLA-4-VCAM-1) pathway may play an important role in the adhesion of T cells to inflamed tissue in rheumatoid arthritis patients. VLA-1 may regulate activity through the CS1 motif of fibronectin. Fibronectin is a glycoprotein found in connective tissue that acts as an adhesive. Researchers examined the interaction of VLA-4 and the CS1 motif of fibronectin. They also examined its affect on the binding of T cells to blood vessels in synovial and lymph gland tissue. The synovium is the membrane that lines the inside of joint cavities. The binding of T cells decreased in the presence of the CS1 peptide and antibody to fibronectin. An antibody that blocked the activity of VCAM-1 also decreased binding significantly. The largest inhibition of binding occurred in the presence of a combination of antibody to VCAM-1 and CS1 peptide or antibody to VLA-4-alpha.
Publication Name: Annals of the Rheumatic Diseases
Subject: Health
ISSN: 0003-4967
Year: 1993
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Dendritic cells and scavenger macrophages in chronic inflammatory bowel disease
Article Abstract:
The gut walls in ten cases of chronic inflammatory bowel disease, including cases of Crohn's disease and ulcerative colitis (inflammation of the mucous of the colon), were studied. Two opposite types of mononuclear phagocytes were identified: scavenger macrophages with blunted projections, and dendritic cells with long dendritic cytoplasmic projections. (Phagocytes are cells which are able to ingest and thereby destroy bacteria, cell debris and other substances.) Dendritic cells were usually found in lymphoid tissue in deep layers of the gut wall. Antigen handling and stimulation of the immune response seem to take place at dendritic cell sites. Scavenger macrophages, on the other hand, were noted in more superficial locations. Ingestion and degradation of foreign material takes place at these spots.
Publication Name: Gut
Subject: Health
ISSN: 0017-5749
Year: 1989
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