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Infection and Immunity, September 2005, p. 5735-5742, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.5735-5742.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Interaction of Bartonella henselae with Endothelial Cells Promotes Monocyte/Macrophage Chemoattractant Protein 1 Gene Expression and Protein Production and Triggers Monocyte Migration

Amy M. McCord, Andrew W. O. Burgess, Melissa J. Whaley, and Burt E. Anderson^*

Department of Medical Microbiology and Immunology, College of Medicine, University of South Florida, Tampa, Florida 33612

Received 15 April 2005/ Returned for modification 5 May 2005/ Accepted 16 May 2005

Bacillary angiomatosis (BA), one of the many clinical manifestations resulting from infection with the facultative intracellular bacterium Bartonella henselae, is characterized by angiogenic lesions. Macrophages have been identified as important effector cells contributing to the angiogenic process during B. henselae infection by infiltrating BA lesions and secreting vascular endothelial growth factor. Monocyte-macrophage chemoattractant protein 1 (MCP-1) recruits macrophages to sites of inflammation. In this study, we investigated the ability of B. henselae to upregulate MCP-1 gene expression and protein production in the human microvascular endothelial cell line HMEC-1. MCP-1 mRNA was induced at 6 and 24 h after treatment with bacteria, whereas protein production was elevated at 6, 24, and 48 h. This induction was not dependent on the presence of bacterial lipopolysaccharide or endothelial cell toll-like receptor 4. However, MCP-1 production was dependent on NF-B activity. Outer membrane proteins of low molecular weight were able to upregulate MCP-1 production. Furthermore, supernatants from B. henselae-infected HMEC-1 were able to induce chemotaxis of THP-1 monocytes. These data suggest a mechanism by which the macrophage effector cell is recruited to the endothelium during B. henselae infection and then contributes to bacterial-induced angiogenesis.

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* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, College of Medicine, University of South Florida, MDC10, 12901 Bruce B. Downs Blvd., Tampa, FL 33612. Phone: (813) 974-2608. Fax: (813) 974-4151. E-mail: banderso{at}hsc.usf.edu.

Editor: J. T. Barbieri

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Infection and Immunity, September 2005, p. 5735-5742, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.5735-5742.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

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