This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Singh, U. P.
Right arrow Articles by Lillard, J. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Singh, U. P.
Right arrow Articles by Lillard, J. W., Jr.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*UniGene
*Compound via MeSH
*Substance via MeSH

 Previous Article  |  Next Article 

Infection and Immunity, August 2007, p. 3722-3728, Vol. 75, No. 8
0019-9567/07/$08.00+0     doi:10.1128/IAI.01770-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Influence of Mycobacterium avium subsp. paratuberculosis on Colitis Development and Specific Immune Responses during Disease{triangledown}

Udai P. Singh,1 Shailesh Singh,2 Rajesh Singh,2 Russell K. Karls,3 Frederick D. Quinn,3 Morris E. Potter,4 and James W. Lillard Jr.1,2*

Department of Microbiology, Biochemistry, and Immunology, Morehouse School of Medicine, Atlanta, Georgia,1 Department of Microbiology and Immunology, University of Louisville, Louisville, Kentucky,2 Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, Georgia,3 Center for Food Safety and Applied Nutrition, Food and Drug Administration, Atlanta, Georgia4

Received 6 November 2006/ Returned for modification 4 January 2007/ Accepted 3 May 2007

The granulomatous and intramural inflammation observed in cases of inflammatory bowel diseases (IBD) and veterinary Johne's disease suggests that Mycobacterium avium subsp. paratuberculosis is a causative agent. However, an incomplete understanding of the immunological steps responsible for the pathologies of IBD makes this conclusion uncertain. Sera from interleukin-10-deficient (IL-10–/–) mice with spontaneous colitis displayed significantly higher M. avium subsp. paratuberculosis-specific immunoglobulin G2a antibody responses than did sera from similar mice without disease. Pathogen-free IL-10–/– mice received control vehicle or the vehicle containing heat-killed or live M. avium subsp. paratuberculosis. Mucosal CD4+ T cells from the mice that developed colitis proliferated and secreted higher levels of gamma interferon and tumor necrosis factor alpha after ex vivo stimulation with a Vß11+ T-cell receptor-restricted peptide from the MPT59 antigen (Ag85B) than those secreted from cells from mice before the onset of colitis. The data from this study provide important information regarding the mechanisms of colitis in IL-10–/– mice, which are driven in part by Ag85B-specific T cells. The data suggest a plausible mechanism of Ag-specific T-cell responses in colitis driven by potent Ags conserved in Mycobacterium species.

* Corresponding author. Mailing address: Brown Cancer Center, Department of Microbiology and Immunology, University of Louisville, 580 S. Preston Street, Baxter II/Room 304C, Louisville, KY 40202. Phone: (502) 852-2174. Fax: (502) 852-3842. E-mail: james.lillard{at}louisville.edu

{triangledown} Published ahead of print on 14 May 2007.

Editor: J. L. Flynn

Infection and Immunity, August 2007, p. 3722-3728, Vol. 75, No. 8
0019-9567/07/$08.00+0     doi:10.1128/IAI.01770-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»