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Pattern of Proinflammatory Cytokine Induction in RAW264.7 Mouse Macrophages Is Identical for Virulent and Attenuated Borrelia burgdorferi¹

Guiqing Wang^2,3,*, Mary M. Petzke^2,*, Radha Iyer^*, Hongyan Wu and Ira Schwartz^4,*

^* Department of Microbiology and Immunology and Department of Medicine, New York Medical College, Valhalla, NY 10595

Lyme disease pathogenesis results from a complex interaction between Borrelia burgdorferi and the host immune system. The intensity and nature of the inflammatory response of host immune cells to B. burgdorferi may be a determining factor in disease progression. Gene array analysis was used to examine the expression of genes encoding cytokines, chemokines, and related factors in the joint tissue of infected C3H/HeJ mice and in a murine macrophage-like cell line in response to a disseminating or attenuated clinical isolate of B. burgdorferi. Both isolates elicited a robust proinflammatory response in RAW264.7 cells characterized by an increase in transcript levels of genes encoding CC and CXC chemokines, proinflammatory cytokines, and TNF superfamily members. Transcription of genes encoding IL-1β, IL-6, MCP-1, MIP-1, CXCR4, and TLR2 induced in RAW264.7 cells by either live or heat-killed spirochetes did not differ significantly at any time point over a 24-h period, nor was there a difference in the protein levels of IL-10, TNF-, IL-6, and IL-12p70 in culture supernatants. Thus, induction of host macrophage expression of proinflammatory mediators by host macrophages does not contribute to the differential pathogenicity of different B. burgdorferi strains.

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 supported by National Institutes of Health Grant AI45801 and Grant 5UO1CI000160 from the Centers for Disease Control and Prevention.

² G.W. and M.M.P. contributed equally to this work.

³ Current address: Department of Pathology, Westchester Medical Center, Clinical Laboratories, Room 1J-04, Valhalla, NY 10595.

⁴ Address correspondence and reprint requests to Dr. Ira Schwartz, Department of Microbiology and Immunology, New York Medical College, BSB Room 308, Valhalla, NY 10595. E-mail address: schwartz{at}nymc.edu

⁵ Abbreviations used in this paper: EM, erythema migrans; BMP, bone morphogenetic protein; BMP-RIB, bone morphogenetic protein receptor IB; COX, cyclooxygenase; GDF, growth differentiation factor; MMP, matrix metalloproteinase; MOI, multiplicity of infection; MMP, matrix metalloproteinase; RST, ribosomal spacer type; TIE, endothelium-specific receptor tyrosine kinase; TIMP, tissue inhibitor of metalloproteinase; TNFSF6, TNF receptor superfamily 6.