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Infection and Immunity, June 2005, p. 3242-3250, Vol. 73, No. 6
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.6.3242-3250.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

ß2 Integrins Control the Severity of Murine Lyme Carditis

Mireia Guerau-de-Arellano,1 Joseph Alroy,2 and Brigitte T. Huber1*

Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts,1 Department of Pathology, Tufts University School of Medicine, Veterinary Medicine and Tufts-NEMC, Boston, Massachusetts2

Received 29 October 2004/ Returned for modification 22 December 2004/ Accepted 21 January 2005

Infection of C57BL/6 (B6) mice with the Lyme disease spirochete Borrelia burgdorferi can result in development of arthritis and carditis. B. burgdorferi induces expression of ß2/CD18 integrins, adhesion molecules that mediate the firm adhesion of leukocytes to the endothelium necessary for cellular extravasation during inflammation. The important role of ß2/CD18 integrins during extravasation suggests that these molecules play a role in the development of Lyme arthritis and carditis. The dependency of these inflammatory processes on the ß2 integrins was investigated in CD18 hypomorph mice, which express low levels of CD18. The results indicate that CD18 deficiency did not abrogate development of Lyme arthritis or carditis. Moreover, it resulted in increased severity of Lyme carditis. B. burgdorferi-infected CD18 hypomorph mice showed an increased macrophage infiltration of the heart, while they produced lower levels of borreliacidal anti-B. burgdorferi antibodies compared to wild-type mice. In accordance with these results, we demonstrate that dendritic cells from CD18 hypomorph mice secrete higher levels of monocyte/macrophage chemoattractant protein 1 (MCP-1/CCL2) in response to B. burgdorferi. Similarly, we show by real-time PCR that B. burgdorferi-infected hearts from CD18 hypomorph mice express increased levels of MCP-1 RNA compared to wild-type mice. Overall, our results indicate that ß2 integrin deficiency does not abrogate B. burgdorferi-induced inflammation; rather, it results in increased recruitment of macrophages into the B. burgdorferi-infected heart, likely due to the increased expression of MCP-1 in this tissue. Thus, ß2 integrins may play a regulatory role in B. burgdorferi-induced inflammation beyond mediating adhesion of leukocytes to the endothelium.

* Corresponding author. Mailing address: Department of Pathology, Tufts University School of Medicine, Jaharis 512, 150 Harrison Ave., Boston, MA 02111. Phone: (617) 636-3989. Fax: (617) 636-0449. E-mail: brigitte.huber{at}tufts.edu.

Editor: J. T. Barbieri

Infection and Immunity, June 2005, p. 3242-3250, Vol. 73, No. 6
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.6.3242-3250.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Dennis, V. A., Dixit, S., O'Brien, S. M., Alvarez, X., Pahar, B., Philipp, M. T. (2009). Live Borrelia burgdorferi Spirochetes Elicit Inflammatory Mediators from Human Monocytes via the Toll-Like Receptor Signaling Pathway. Infect. Immun. 77: 1238-1245 [Abstract] [Full Text]  
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  • Behera, A. K., Hildebrand, E., Uematsu, S., Akira, S., Coburn, J., Hu, L. T. (2006). Identification of a TLR-Independent Pathway for Borrelia burgdorferi-Induced Expression of Matrix Metalloproteinases and Inflammatory Mediators through Binding to Integrin {alpha}3beta1. J. Immunol. 177: 657-664 [Abstract] [Full Text]  
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