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Infection and Immunity, March 2002, p. 1372-1381, Vol. 70, No. 3
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.3.1372-1381.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Role of Osteopontin in Murine Lyme Arthritis and Host Defense against Borrelia burgdorferi

Melissa R. Potter,1,{dagger} Susan R. Rittling,2 David T. Denhardt,2 Randall J. Roper,3 John H. Weis,1 Cory Teuscher,3 and Janis J. Weis1*

Department of Pathology, Division of Cell Biology and Immunology, University of Utah School of Medicine, Salt Lake City, Utah 84132-2501,1 Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, New Jersey 08854-8082,2 Department of Veterinary Pathobiology, University of Illinois at Urbana-Champaign, Urbana, Illinois 618023

Received 4 October 2001/ Returned for modification 19 November 2001/ Accepted 18 December 2001

Several genetic loci in the mouse have been identified that regulate the severity of Lyme arthritis. The region of chromosome 5 including the osteopontin (OPN) gene (Opn) has been identified in intercross populations of C3H/HeN x C57BL/6 and C3H/HeJ x BALB/cAnN mice. OPN is of particular interest as it is involved in the maintenance and remodeling of tissue during inflammation, it regulates production of interleukin-10 (IL-10) and IL-12 (cytokines implicated in Lyme arthritis), it is necessary for host control of certain bacterial infections, and mice displaying different severities of Lyme arthritis possess different alleles of the OPN gene. Macrophages and splenocytes from OPN-deficient mice on mixed C57BL/6J-129S or inbred 129S backgrounds were stimulated with the Pam3Cys modified lipoprotein from Borrelia burgdorferi, OspA. OPN was not required for OspA-induced cytokine production; however, macrophages from 129S-Opn-/- mice displayed a reduced level of IL-10 production. OPN was also not required for resistance to severe arthritis, as B. burgdorferi-infected 129S-Opn-/- mice developed mild arthritis, as did their wild-type littermates. Arthritis was more severe in OPN-deficient mice on the mixed C57BL/6J-129S backgrounds than in inbred mice of either strain. This increase was most likely due to a gene(s) closely linked to Opn on chromosome 5 in conjunction with other randomly assorting genes. Deficiency in OPN did not influence the numbers of spirochetes in tissues from B. burgdorferi-infected mice, indicating OPN is not part of the host defense to this pathogen. Interestingly, there was no alteration in the B. burgdorferi-specific antibody isotypes in OPN-deficient mice, indicating that its effect on helper T-cell responses is not relevant to the host response to B. burgdorferi.

* Corresponding author. Mailing address: Dept. of Pathology, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132-2501. Phone: (801) 581-8386. Fax: (801) 581-4517. E-mail: janis.weis{at}path.utah.edu.

{dagger} Present address: New York City Dept. of Health, Office of the Chief Medical Examiner, Dept. of Forensic Biology, New York, NY 10016-6402.

Infection and Immunity, March 2002, p. 1372-1381, Vol. 70, No. 3
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.3.1372-1381.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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