IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Potter, M. R.
Right arrow Articles by Weis, J. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Potter, M. R.
Right arrow Articles by Weis, J. J.

 Previous Article  |  Next Article 

Infection and Immunity, October 2000, p. 5603-5609, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Interleukin-4 (IL-4) and IL-13 Signaling Pathways Do Not Regulate Borrelia burgdorferi-Induced Arthritis in Mice: IgG1 Is Not Required for Host Control of Tissue Spirochetes

Melissa R. Potter,1 Nancy Noben-Trauth,2 John H. Weis,1 Cory Teuscher,3 and Janis J. Weis1,*

Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah 841321; Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-18922; and Department of Veterinary Pathobiology, University of Illinois at Urbana-Champaign, Urbana, Illinois 618023

Received 6 April 2000/Returned for modification 8 June 2000/Accepted 30 June 2000

Previous studies have suggested that interleukin-4 (IL-4) has a protective effect in host defense to Borrelia burgdorferi infection, both in limiting the severity of arthritis and in controlling spirochete numbers in tissues, and a mapping study revealed suggestive linkage to a cluster of genes on mouse chromosome 11, including the genes for IL-4 and IL-13. In contrast, other studies have questioned the importance of IL-4. In this study the involvement of IL-4 in murine Lyme disease was examined in C57BL/6J and BALB/cJ mice with targeted disruptions in the IL-4 gene, the IL-4Ralpha chain gene, or both. A spectrum of arthritis severity was seen in BALB/cJ mice, and ablation of IL-4, IL-4Ralpha , or both had no effect on the overall severity of arthritis as determined by joint swelling and histopathology. Wild-type C57BL/6J mice exhibited mild to moderate arthritis, and ablation of IL-4 again had no effect on arthritis severity. IL-4- and IL-4Ralpha -deficient mice produced extremely low levels of immunoglobulin G1 (IgG1) and showed increased production of IgG2b. This shift in immunoglobulin isotype had no effect on the host's ability to control spirochete growth in either strain of mouse, as determined by PCR detection of B. burgdorferi DNA from heart and ankle tissues. In summary, the IL-4-IL-4Ralpha pathway, including IL-13 signaling, neither limits arthritis severity nor is required for control of spirochete growth during B. burgdorferi infection of mice. Furthermore, the IgG1 isotype is not required to control B. burgdorferi cell numbers in tissues. These findings suggest the host defense against B. burgdorferi infection is not dependent on the Th1-Th2 paradigm of T-cell responses.

* Corresponding author. Mailing address: University of Utah School of Medicine, Department of Pathology, 50 North Medical Drive, Salt Lake City, UT 84132. Phone: (801) 581-8386. Fax: (801) 581-4517. E-mail: janis.weis{at}path.med.utah.edu.

Infection and Immunity, October 2000, p. 5603-5609, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2000 by the American Society for Microbiology. All rights reserved.