作者: Guiqing Wang , Mary M. Petzke , Radha Iyer , Hongyan Wu , Ira Schwartz
DOI: 10.4049/JIMMUNOL.180.12.8306
关键词: Regulation of gene expression 、 TLR2 、 Biology 、 Borrelia burgdorferi 、 Chemokine 、 Virulence 、 Proinflammatory cytokine 、 Immune system 、 Immunology 、 Cell culture
摘要: Lyme disease pathogenesis results from a complex interaction between Borrelia burgdorferi and the host immune system. The intensity nature of inflammatory response cells to B. may be determining factor in progression. Gene array analysis was used examine expression genes encoding cytokines, chemokines, related factors joint tissue infected C3H/HeJ mice murine macrophage-like cell line disseminating or attenuated clinical isolate burgdorferi. Both isolates elicited robust proinflammatory RAW264.7 characterized by an increase transcript levels CC CXC TNF superfamily members. Transcription IL-1beta, IL-6, MCP-1, MIP-1alpha, CXCR4, TLR2 induced either live heat-killed spirochetes did not differ significantly at any time point over 24-h period, nor there difference protein IL-10, TNF-alpha, IL-12p70 culture supernatants. Thus, induction macrophage mediators macrophages does contribute differential pathogenicity different strains.