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Infection and Immunity, October 2003, p. 5556-5564, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.5556-5564.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

The Urokinase Receptor Can Be Induced by Borrelia burgdorferi through Receptors of the Innate Immune System

James L. Coleman1,2 and Jorge L. Benach2*

State of New York Department of Health,1 Center for Infectious Diseases, Stony Brook University, Stony Brook, New York 11794-51202

Received 18 June 2003/ Returned for modification 11 July 2003/ Accepted 24 July 2003

Monocytic cells exposed to Borrelia burgdorferi, through unknown receptors, overexpress the urokinase receptor (uPAR), a key mediator of the plasminogen activation system. We show that combined blockade of CD14 and TLR2 causes a significant inhibition of B. burgdorferi-induced uPAR in Mono Mac 6 (MM6) cells. Other pattern recognition receptors tested (CD11b/CD18, the mannose receptor, and the N-formyl-methionyl-leucyl-phenylalanine receptor) did not have demonstrated roles in B. burgdorferi-mediated uPAR induction. We dissected the result for CD14 andTLR2 by investigating the singular contributions of each. Independent functional blockade of CD14 or TLR2 failed to inhibit B. burgdorferi-mediated uPAR induction. 1,25-Dihydroxyvitamin D3 differentiation of MM6 cells increased CD14 expression 12-fold but did not augment B. burgdorferi-mediated uPAR expression. Peritoneal exudate macrophages (PEM) from CD14- or TLR2-deficient mice were not defective in B. burgdorferi-mediated synthesis of uPAR mRNA and protein. Increased uPAR mRNA or protein or both were apparent in PEM from transgenic and control mice, even at a ratio of one Borrelia spirochete per cell. We conclude that signaling for the uPAR response, as mediated by B. burgdorferi, proceeds with CD14 and TLR2 as partial contributors. That part under control of CD14 and TLR2 represents a new link between the host plasminogen activation and innate immunity systems.

* Corresponding author. Mailing address: Center for Infectious Diseases, 248 Centers for Molecular Medicine, Stony Brook University, Stony Brook, NY 11794-5120. Phone: (631) 632-4286. Fax: (631) 632-4294. E-mail: jbenach{at}notes.cc.sunysb.edu.

Editor: J. T. Barbieri

Infection and Immunity, October 2003, p. 5556-5564, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.5556-5564.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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