Intracellular TLR7 is activated in human oligodendrocytes in response to Borrelia burgdorferi exposure.

摘要: Lyme neuroborreliosis, caused by the gram-negative bacterium Borrelia burgdorferi, may affect central and/or peripheral nervous systems. In previous studies, we showed that human oligodendrocytes exposed to bacteria undergo apoptosis in an inflammatory environment, and pathways trigger cell-death pathways. We further demonstrated several receptor tyrosine kinases were involved triggering downstream effects, leading inflammation apoptosis. Toll-like receptors TLR2 TLR5, which are commonly studied disease, only had a minimal role processes. To delineate of other TLRs, if any, real-time RT-PCR array experiments carried out as initial screen. Along with genes, TLR7 mRNA was upregulated cells B. burgdorferi. Further analysis immunohistochemistry protein is present readily detectable amounts, although no discernible differences could be seen between medium burgdorferi-exposed this technique. Nevertheless, use specific inhibitors siRNA inducing IL-6 CCL2 dose dependent manner, likely CXCL8. Triggering intracellular such TLR7, senses RNA, typically non-phagocytic indicates either niche for inside cell or novel uptake nucleic acids initiate responses.