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.

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Title: 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.
Title Abreviation: Gut		Date of Pub: 1990 May
Author: Seldenrijk CA; Drexhage HA; Meuwissen SG; Meijer CJ;
Issue/Part/Supplement: 5	Volume Issue: 31		Pagination: 529-35
MESH Headings: Adult; Aged; Aged, 80 and over; Antigens, Bacterial (IM); Colitis, Ulcerative (IM); Crohn Disease (IM); Female; Human; Immunity, Cellular; Macrophage Migration-Inhibitory Factors (AN); Male; Middle Age; Mycobacterium (IM); Mycobacterium tuberculosis (IM); Mycobacterium, Atypical (IM); T-Lymphocytes (IM);
Journal Title Code: FVT	Publication Type: JOURNAL ARTICLE
Date of Entry: 900719N	Entry Month: 9009
Country: ENGLAND	Index Priority: 1
Language: Eng	Unique Identifier: 90276896
Unique Identifier: 90276896	ISSN: 0017-5749
Abstract: A mycobacterial aetiology has been suggested for Crohn's disease. A slow growing mycobacterium, biochemically and genetically identical to M paratuberculosis, the causative agent of enteritis in ruminants (Johne's disease), has been isolated from gut specimens of patients affected by Crohn's disease. If M paratuberculosis or other mycobacteria play a role in the pathogenesis of Crohn's disease, then patients may have been sensitised to these mycobacteria or show an anergy immune reaction. We therefore investigated the T-cell mediated immune response to sonicates of M paratuberculosis, M kansasii, M avium, and M tuberculosis in 35 patients with Crohn's disease, 28 with ulcerative colitis, and 25 controls using a macrophage inhibition factor assay on peripheral blood lymphocytes. Two types of reaction patterns were identified--that is, 'responders' (subjects with a macrophage inhibition factor assay in which a dose response relation was present and a percentage of inhibition exceeding 20%), and 'non-responders'. There was no significant difference in the prevalence of responders (59%-80%) and non-responders (20%-41%) to these mycobacteria between the group of Crohn's disease, ulcerative colitis, and control group. We found also that a large proportion of controls showed T-cell immunisation to the mycobacteria which supports the contention that the antigens are practically commensal. Our results do not support the proposed involvement of mycobacteria in the pathogenesis of Crohn's disease.
Abstract By: Author
Address: Department of Pathology, Free University Hospital of Amsterdam, The Netherlands.