期刊
MOLECULAR PAIN
卷 14, 期 -, 页码 -出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/1744806918808150
关键词
Neuropathic pain; neuroinflammation; CD11b; Src; TLR4
资金
- National Natural Science Foundation of China [81371253, 81671079]
- Research Foundation of Shanghai Science and Technology Commission [17XD1424300/16411967300]
- TCM Supported Project from Science and Technology Commission of Shanghai Municipality [15401900800]
Neuroinflammation plays an important role in the induction and maintenance of chronic pain. Orchestra of pattern-recognition receptor-induced pro-inflammatory and anti-inflammatory cytokines is critical for inflammation homeostasis. CD11b on macrophages could inhibit toll-like receptor (TLR) activation-induced inflammatory responses. However, the function of CD11b on microglia remains unknown. In the current study, we demonstrated that CD11b-deficient microglia cells produced more inflammatory cytokines, such as interleukin-6 and tumor necrosis factor alpha, while less anti-inflammatory cytokines. Signal transduction assay confirmed that nuclear factor-kappa B activation was increased in CD11b-deficient microglia cells, which resulted from decreased activation of Src. Inhibition of Src by PP1 increased inflammation in wild-type microglia cells significantly, but not in CD11b-deficient microglia cells. In vivo, CD11b-deficient mice were more susceptible to chronic constrictive injury-induced allodynia and hyperalgesia with significantly more inflammatory cytokines expression. All these results indicated that the regulatory function of CD11b-Src signal pathway on both inflammatory and anti-inflammatory cytokines in microglia cells is a potential target in neuropathic pain treatment.
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