Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 12, Pages 8306-8315Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.12.8306
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Funding
- NIAID NIH HHS [R01 AI045801, R01 AI045801-08, AI 45801] Funding Source: Medline
- NCPDCID CDC HHS [U01 CI000160, 5 U01 CI 000160] Funding Source: Medline
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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-1 beta, IL-6, MCP-1, MIP-1 alpha, 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-alpha, 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.
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