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Infection and Immunity, February 2007, p. 613-620, Vol. 75, No. 2
0019-9567/07/$08.00+0     doi:10.1128/IAI.00685-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Recruitment of Macrophages and Polymorphonuclear Leukocytes in Lyme Carditis{triangledown}

Ruth R. Montgomery,1* Carmen J. Booth,2 Xiaomei Wang,1 Victoria A. Blaho,3 Stephen E. Malawista,1 and Charles R. Brown3

Department of Internal Medicine,1 Section of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut 06510,2 Departments of Veterinary Pathobiology and Molecular Microbiology and Immunology, University of Missouri, Columbia, Missouri3

Received 28 April 2006/ Returned for modification 31 July 2006/ Accepted 1 November 2006

Lyme arthritis, caused by the spirochete Borrelia burgdorferi, can be recurrent or prolonged, whereas Lyme carditis is mostly nonrecurring. A prominent difference between arthritis and carditis is the differential representation of phagocytes in these lesions: polymorphonuclear leukocytes (PMN) are more prevalent in the joint, and macrophages predominate in the heart lesion. We have previously shown differential efficiency of B. burgdorferi clearance by PMN and macrophages, and we now investigate whether these functional differences at the cellular level may contribute to the observed differences in organ-specific pathogenesis. When we infected mice lacking the neutrophil chemokine receptor (CXCR2–/– mice) with spirochetes, we detected fewer PMN in joints and less-severe arthritis. Here we have investigated the effects of the absence of the macrophage chemokine receptor CCR2 on the development and resolution of Lyme carditis in resistant (C57BL/6J [B6]) and sensitive (C3H/HeJ [C3H]) strains of mice. In B6 CCR2–/– mice, although inflammation in hearts is mild, we detected an increased burden of B. burgdorferi compared to that in wild-type (WT) mice, suggesting reduced clearance in the absence of macrophages. In contrast, C3H CCR2–/– mice have severe inflammation but a decreased B. burgdorferi burden compared to that in WT C3H mice both at peak disease and during resolution. Histopathologic examination of infected hearts revealed that infected C3H CCR2–/– animals have an increased presence of PMN, suggesting compensatory mechanisms of B. burgdorferi clearance in the hearts of infected C3H CCR2–/– mice. The more efficient clearance of B. burgdorferi from hearts by CCR2–/– versus WT C3H mice suggests a natural defect in the recruitment or function of macrophages in C3H mice, which may contribute to the sensitivity of this strain to B. burgdorferi infection.

* Corresponding author. Mailing address: Department of Internal Medicine, Yale University School of Medicine, 300 Cedar St./TAC S413, New Haven, CT 06520-8031. Phone: (203) 785-7039. Fax: (203) 785-7053. E-mail: ruth.montgomery{at}yale.edu.

{triangledown} Published ahead of print on 13 November 2006.

Editor: J. L. Flynn

Infection and Immunity, February 2007, p. 613-620, Vol. 75, No. 2
0019-9567/07/$08.00+0     doi:10.1128/IAI.00685-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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