Lack of mycobacterial DNA in Crohn's disease tissue

Wu, Shiji; Pao, Chia C.; Chan, John; Yen, Timothy

doi:10.1016/0140-6736(91)90837-f

Cited by 36 publications

(19 citation statements)

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“…Perhaps there is something protective in ingesting unpasteurized milk or well water against developing either Crohn's dis-VOL. 42,2004 CROHNЈS DISEASE AND M. PARATUBERCULOSIS SEROPREVALENCE 1133 ease or ulcerative colitis. This may support a hypothesis regarding access to various organisms in childhood as being protective against later development of autoimmune-like disease.…”

Section: Discussionmentioning

confidence: 99%

Population-Based Case Control Study of Seroprevalence ofMycobacterium paratuberculosisin Patients with Crohn's Disease and Ulcerative Colitis

Bernstein¹,

Blanchard

Rawsthorne³

et al. 2004

J Clin Microbiol

102

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There is renewed enthusiasm for exploring the possibility that Mycobacterium paratuberculosis may be causative in Crohn's disease (CD). We aimed to determine whether CD subjects are more likely to be M. paratuberculosis seropositive than controls. Using our population-based University of Manitoba Inflammatory Bowel Disease Research Registry, we recruited CD and ulcerative colitis (UC) subjects between 18 and 50 years of age for a study involving detailed questionnaires and venipuncture. We accessed the population-based databases of Manitoba Health (single provincial health insurer) to get age-, gender-, and geography-matched controls to our inflammatory bowel disease (IBD) population. We asked enrolling IBD subjects for potential nonaffected sibling controls. We used an enzyme-linked immunosorbent assay (ELISA) for serum antibodies to M. paratuberculosis initially developed for cattle but adapted for human use. The rate of positive ELISA results, based on previously published interpretation criteria, was significantly higher for all study groups. There was no difference in M. paratuberculosis seropositivity rate among CD patients (37.8%; n ‫؍‬ 283), UC patients (34.7%; n ‫؍‬ 144), healthy controls (33.6%; n ‫؍‬ 402), and nonaffected siblings (34.1%; n ‫؍‬ 138). For siblings, there was no correlation between M. paratuberculosis serological status and that of the corresponding IBD affected sibling. None of the demographic or questionnaire variables studied were predictive of M. paratuberculosis status. Subjects with CD and UC were less likely to have ingested unpasteurized milk and less likely to have had a non-tap water source as a primary water source. In conclusion, in this population-based case control study, the M. paratuberculosis seropositivity rate was approximately 35% for all groups and there was no difference in rates between CD patients, UC patients, healthy controls, or nonaffected siblings. The much higher rate of seropositivity for subjects from Manitoba, Canada, than for those from Denmark or Wisconsin cannot be obviously explained. While these data seem to refute any association of CD with M. paratuberculosis, the high seroprevalence in Manitobans raises the possibility that the high rates of CD in Manitoba could be related to high exposure rates for M. paratuberculosis. Hence, the possibility of an association between M. paratuberculosis and CD remains inconclusive.

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Section: Discussionmentioning

confidence: 99%

Population-Based Case Control Study of Seroprevalence ofMycobacterium paratuberculosisin Patients with Crohn's Disease and Ulcerative Colitis

Bernstein¹,

Blanchard

Rawsthorne³

et al. 2004

J Clin Microbiol

102

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“…Acetic acid fixation of therapeutically resected specimens has made these lymphoid tissues easily visible. 17,27 Studies of detection of M. paratuberculosis by PCR in Crohn's disease [7][8][9][10][11][12][28][29][30][31] can be categorized into four groups. In the first and second groups, the agent was detected more often in Crohn's disease than in ulcerative colitis or controls.…”

Section: Discussionmentioning

confidence: 99%

“…10,11 Another group was unable to detect the agent. 12 In this study we attempted to clarify this controversy by determining whether M. paratuberculosis was detected in intestinal tissue in Crohn's disease and, with special regard to its etiological significance, we examined the sites where M. paratuberculosis invades and where early lesions appear. M. paratuberculosis is known to invade at the site of Peyer's patches via the M cells 13 and to cause the earliest lesions in animal models.…”

Section: Introductionmentioning

confidence: 99%

No Mycobacterium paratuberculosis detected in intestinal tissue, including Peyer's patches and lymph follicles, of Crohn's disease

Chiba

Fukushima

Horie

et al. 1998

Journal of Gastroenterology

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To clarify the etiologic significance of Mycobacterium paratuberculosis in Crohn's disease, we investigated whether M. paratuberculosis was detected in intestinal tissues, including Peyer's patches, where M. paratuberculosis invades, and colonic lymph follicles, where early lesions appear. Fifty-one samples of intestinal tissues, either therapeutically resected or biopsied, including 34 specimens from 30 patients with Crohn's disease, were studied. Four Peyer's patches and eight lymph follicles were included in the intestinal tissue samples of Crohn's disease. They were visualized by acetic acid fixation. DNA extracted from intestinal tissues by proteinase K treatment was used for nested polymerase chain reaction (PCR) for detection of IS900, which is specific for M. paratuberculosis. PCR products were analyzed by agarose gel electrophoresis and subsequent Southern blot analysis. Our amplification system could detect 7.5 fg of M. paratuberculosis DNA. None of the tissue samples showed positive IS900 amplification, whereas they all showed amplification of the positive control human leukocyte antigen (HLA)-DQA DNA. Spiked experiments of tissue samples with M. paratuberculosis demonstrated that inhibitors of IS900 amplification were not present in the samples. Our study does not support the etiologic significance of M. paratuberculosis in Crohn's disease.

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“…paratubercuhsis from patients with CD [10] sparked renewed interest in this organism in relation to CD. However, detection of mycobacterial DNA in CD tissue by amplification using Ihe polymerase chain reaction (PCR) has produced conflicting results [11][12][13][14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Peripheral cell-mediated immune response to mycobacterial antigens in inflammatory bowel disease

Rowbotham

Howdle

Trejdosiewicz

1995

Clinical and Experimental Immunology

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SUMMARYA mycobacterial etiology has been proposed In Crohn's disease (CD). We have sought evidence of increased or modified T lymphocyte immune responses to Mycnhactcrium tuberculosis and Myco. paratubercuhsis in patients with CD (ti = 13), compared with ulcerative colitis (UC; n = 17) and controls (« = 17). Peripheral blood cells were cultured with phytohaemagglutinin (positive mitogen control), mycobacterial purified protein derivative (PPD) preparations, lysates., column fractions and whole, heat-killed bacteria. Responses of T cells and T cell subsets were assessed by expression of activation markers (CD25. CD69). coupled with blast ogenesis assays (^H-thymidine uptake) and estimates of proliferation. Virtually all patients responded to Myco. paratuberculo.\is and Myco. tuberculosis antigens. There were no significant differences between patient groups, although there was a very high overall correlation (r = 095; P<0000\) between responses to the two mycobacterial species. Most of the activation and proliferative responses resided in the CD4'*' (T helper) subset. Although up to 15% of CDS"^ (suppressor/cytotoxic) cells also became activated, the CD8^ cells did not proliferate subsequently. Cells expressing the alternate y/) form of the T cell receptor (TCR 7(S^)did not activate or proliferate in response to mycobacterial antigens. There were no differences in any of these parameters between patient groups. We conclude that there is no specilic increase or alteration in cell-mediated anti-mycobacterial immunity in inflammatory bowel disease (IBD). Thus our data do not suppwrt a mycobacterial etiopathology of Crohn's disease.

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Lack of mycobacterial DNA in Crohn's disease tissue

Cited by 36 publications

References 0 publications

Population-Based Case Control Study of Seroprevalence ofMycobacterium paratuberculosisin Patients with Crohn's Disease and Ulcerative Colitis

Population-Based Case Control Study of Seroprevalence ofMycobacterium paratuberculosisin Patients with Crohn's Disease and Ulcerative Colitis

No Mycobacterium paratuberculosis detected in intestinal tissue, including Peyer's patches and lymph follicles, of Crohn's disease

Peripheral cell-mediated immune response to mycobacterial antigens in inflammatory bowel disease

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