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Infection and Immunity, June 2002, p. 3164-3169, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.3164-3169.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Mice Lacking Monocyte Chemoattractant Protein 1 Have Enhanced Susceptibility to an Interstitial Polymicrobial Infection Due to Impaired Monocyte Recruitment

P. Chae,1 M. Im,2 F. Gibson,3 Y. Jiang,1 and D. T. Graves4*

Department of Endodontics,1 Department of Periodontology and Oral Biology, Boston University School of Dental Medicine,4 Department of Infectious Disease, Boston Medical Center, Boston, Massachusetts,3 Department of Conservative Dentistry, College of Dentistry Wonkwang University, Iksan City, South Korea2

Received 28 September 2001/ Returned for modification 4 January 2002/ Accepted 22 February 2002

Monocyte chemoattractant protein 1 (MCP-1) is an important chemokine that induces monocyte recruitment in a number of different pathologies, including infection. To investigate the role of MCP-1 in protecting a host from a chronic interstitial polymicrobial infection, dental pulps of MCP-1-/- mice and controls were inoculated with six different oral pathogens. In this model the recruitment of leukocytes and the impact of a genetic deletion on the susceptibility to infection can be accurately assessed by measuring the progression of soft tissue necrosis and osteolytic lesion formation. The absence of MCP-1 significantly impaired the recruitment of monocytes, which at later time points was threefold higher in the wild-type mice than in MCP-1-/- mice (P < 0.05). The consequence was significantly enhanced rates of soft tissue necrosis and bone resorption (P < 0.05). We also determined that the MCP-1-/- mice were able to recruit polymorphonuclear leukocytes (PMNs) to a similar or greater extent as controls and to produce equivalent levels of Porphyromonas gingivalis-specific total immunoglobulin G (IgG) and IgG1. These results point to the importance of MCP-1 expression and monocyte recruitment in antibacterial defense and demonstrate that antibacterial defense is not due to an indirect effect on PMN recruitment or modulation of the adaptive immune response.

* Corresponding author. Mailing address: Boston University School of Dental Medicine, W202D, 700 Albany Street, Boston, MA 02118. Phone: (617) 638-8547. Fax: (617) 638-4924. E-mail: dgraves{at}bu.edu.

Editor: R. N. Moore

Infection and Immunity, June 2002, p. 3164-3169, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.3164-3169.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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