The contributing role of CD14 in toll-like receptor 4 dependent neuropathic pain.
作者： L. Cao , F.Y. Tanga , J.A. DeLeo
DOI: 10.1016/J.NEUROSCIENCE.2008.10.004
关键词:
摘要: We have previously demonstrated that CNS toll-like receptor 4 (TLR4) plays a key role in the development of behavioral hypersensitivity rodent model neuropathic pain, spinal nerve L5 transection (L5Tx). TLR4 is well-known for lipopolysaccharide (LPS) innate immune responses. In current study, we further investigated CD14, an accessory molecule LPS-TLR4 signaling pathway, L5Tx-induced pain. CD14 knockout (KO) mice displayed significantly decreased sensitivity (mechanical allodynia and thermal hyperalgesia) as early day 1 post-L5Tx, indicating nociceptive CD14. By flow cytometric analyses, observed elevated microglial surface expression ipsilateral lumbar cord 3 days well remarkable increases size (via forward scatter (FSC)) granularity side (SSC)). Further, intrathecal injection soluble induced greater mechanical wild type (C3H/HeN) compared with TLR4-deficient (C3H/HeJ) mice. Together, these data demonstrate contributing TLR4-dependent injury-induced
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