Borrelia burgdorferi activates nuclear factor-kappa B and is a potent inducer of chemokine and adhesion molecule gene expression in endothelial cells and fibroblasts.

摘要: Lyme disease, caused by the tick-borne spirochete Borrelia burgdorferi, is a systemic infection with preponderance for skin, joints, heart, and nervous system. Inflammatory lesions of target organs are characterized presence spirochetes inflammatory leukocytes. We have analyzed potential B. burgdorferi to induce gene expression chemokines adhesion molecules in human endothelial cells, keratinocytes, fibroblasts. find induction RANTES (regulated upon activation, normal T cells expressed secreted), monocyte chemoattractant protein-1, IL-8, gro-alpha, IFN-inducible protein-10, mig (monokine induced gamma-IFN), E-selectin, ICAM-1, VCAM-1 same ICAM-1 This mediated lipid moiety outer surface lipoprotein A. Induction chemokine molecule genes occurs rapidly does not require new protein synthesis. blocked inhibitors nuclear factor (NF)-kappa also that induces translocation NF-kappa B transient increase its inhibitor I kappa B-alpha. These findings indicate potent inducer required leukocyte recruitment foci, data suggest this biologic activity due ability activate pleiotropic transcription