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The germfree state prevents development of gut and joint inflammatory disease in HLA-B27 transgenic rats.

Open access
Taurog, J D, Richardson, J A, Croft, J T, Simmons, W A, Zhou, M, Fernández-Sueiro, J L, Balish, E, Hammer, R E·1994·The Journal of experimental medicine

Abstract

A number of inflammatory disease states occur with greatly increased frequency in individuals inheriting the human major histocompatibility complex class I allele HLA-B27. In a minority of cases, namely those with B27-associated reactive arthritis, there is good evidence that the disease state is triggered by infection with an enteric or genitourinary bacterial pathogen. For the majority of B27-associated disease, no definite pathogenetic role for bacteria has been established. However, in these latter cases intestinal inflammation can often be demonstrated, and it sometimes occupies a major part of the clinical picture. Rats transgenic for B27 are known to develop a disorder resembling B27-associated human disease, with prominent intestinal, joint, skin, and male genital inflammatory lesions. We report here that B27 transgenic rats raised in a germfree environment do not develop inflammatory intestinal or peripheral joint disease, whereas the skin and genital inflammatory lesions are unaffected by the germfree state. These findings support the concept that gut and joint inflammation are pathogenetically closely related, and they provide direct evidence that the commensal gut flora play an important role in the pathogenesis of B27-associated gut and joint inflammation.

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Metadata

Authors
Taurog, J. D., Richardson, J. A., Croft, J. T., Simmons, W. A., Zhou, M., Fernández-Sueiro, J. L., Balish, E., & Hammer, R. E.
Venue
The Journal of experimental medicine
Published
1994-12-01
Volume
180
Issue
6
Pages
2359-2364
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2137109050
Cited by
1,156
References
0
FWCI
20.81
Type
journal article
Language
en
Open access
bronze

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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