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Increasing the Recruitment of Neutrophils to the Site of Infection Dramatically Attenuates Borrelia burgdorferi Infectivity¹

Qilong Xu^*, Sunita V. Seemanapalli^*, Kathryn E. Reif^*, Charles R. Brown and Fang Ting Liang^2,*

^* Department of Pathobiological Sciences, Louisiana State University, Baton Rouge, LA 70803; and Departments of Molecular Microbiology and Immunology and Veterinary Pathobiology, University of Missouri, Columbia, MO 65211

Borrelia burgdorferi infection causes an initial skin lesion called erythema migrans (EM) in human Lyme disease and in models of monkey and rabbit borreliosis. EM results from the inflammatory response triggered by spirochete replication and likely develops to contain the initial infection but allows bacterial dissemination to occur. The essential lack of neutrophil involvement in EM histopathology prompted us to examine the consequence of increasing their recruitment in the inflammatory response to the Lyme disease agent. B. burgdorferi was modified genetically to constitutively express and secrete the chemokine KC, a neutrophil chemoattractant. After inoculation into the dermis of the murine host, control spirochetes induced an infiltration of macrophages, neutrophils, and basophils within 6 h; however, the recruited neutrophils and basophils were quickly substituted by eosinophils, and the inflammatory response became macrophage dominant by 16 h. Such a response failed to contain the initial infection and allowed the spirochetes to disseminate. In contrast, B. burgdorferi with KC secretion induced an intensive neutrophil infiltration at the inoculation site, and as a result, the host’s ability to control the initial infection was greatly enhanced. Taken together, this study suggests that the failure of sufficient neutrophil recruitment and activation during the initial inflammatory response may allow B. burgdorferi to effectively colonize the mammalian host.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was in part supported by National Institutes of Health AR052748 (to C.R.B.), and a National Institutes of Health/National Institute of Arthritis and Musculoskeletal and Skin Diseases Career Development Award and an Arthritis Foundation Investigators Award (both to F.T.L.).

² Address correspondence and reprint requests to Dr. Fang Ting Liang, Department of Pathobiological Sciences, Louisiana State University, Skip Bertman Drive, Baton Rouge, LA 70803. E-mail address: fliang{at}vetmed.lsu.edu

³ Abbreviation used in this paper: EM, erythema migran.

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