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Anaplasma phagocytophilum-Borrelia burgdorferi Coinfection Enhances Chemokine, Cytokine, and Matrix Metalloprotease Expression by Human Brain Microvascular Endothelial Cells

Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287,¹ Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205²

Received 26 July 2007/ Returned for modification 12 September 2007/ Accepted 19 September 2007

Borrelia burgdorferi and Anaplasma phagocytophilum coinfect and are transmitted by Ixodes species ticks. Clinical indicators suggest that A. phagocytophilum coinfection contributes to the severity, dissemination, and, possibly, sequelae of Lyme disease. Previous in vitro studies showed that spirochete penetration through human brain microvascular endothelial cells of the blood-brain barrier is facilitated by endothelial cell-derived matrix metalloproteases (MMPs). A. phagocytophilum-infected neutrophils continuously release MMPs and other vasoactive biomediators. We examined B. burgdorferi infection of brain microvascular barriers during A. phagocytophilum coinfection and showed that coinfection enhanced reductions in transendothelial electrical resistance and enhanced or synergistically increased production of MMPs (MMP-1, -3, -7, -8, and -9), cytokines (interleukin 6 [IL-6], IL-10, and tumor necrosis factor alpha), and chemokines (IL-8 and macrophage inflammatory protein 1) known to affect vascular permeability and inflammatory responses.

Published ahead of print on 26 September 2007.

^# Present address: Department of Oceanography and Fisheries, University of Ghana, Legon, Accra, Ghana.

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