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Antimicrobial Agents and Chemotherapy, October 2009, p. 4490-4494, Vol. 53, No. 10
0066-4804/09/$08.00+0 doi:10.1128/AAC.00558-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

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Patricia A. Rosa
Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, NIAID, NIH, 903 S. 4th St., Hamilton, Montana 59840
Received 25 April 2009/ Returned for modification 19 June 2009/ Accepted 23 July 2009
We hypothesize a potential role for Borrelia burgdorferi OspC in innate immune evasion at the initial stage of mammalian infection. We demonstrate that B. burgdorferi is resistant to high levels (>200 µg/ml) of cathelicidin and that this antimicrobial peptide exhibits limited binding to the spirochetal outer membrane, irrespective of OspC or other abundant surface lipoproteins. We conclude that the essential role of OspC is unrelated to resistance to this component of innate immunity.
Published ahead of print on 3 August 2009.
Present address: Division of Biological Sciences, University of Montana, 32 Campus Drive 4824, Missoula, MT 59812.
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