A TLR-CXCL1 pathway in DRG neurons induces neutrophil accumulation in the DRG and mechanical allodynia in EAE mice.

Multiple sclerosis (MS) is a potentially disabling disease of the central nervous system. Approximately half of the patients with MS experience severe pain; However, currently available therapies provide only enough assistance. The mechanisms underlying the generation of neuropathic pain in patients with MS is not fully understood. More recently, we found that the neutrophil elastase of the accumulation of neutrophils in mechanical allodynia dorsal root ganglion (DRG) neurons and induces sensitive DRG in a mouse model of experimental autoimmune encephalomyelitis (EAE).

However, the underlying mechanisms of accumulation of neutrophils in DRG after myelin oligodendrocyte glycoprotein (MOG35-55, an immunogenic peptide) immunization is still unclear. Here, we found that the C-X-C motif ligand 1 (CXCL1) is regulated in DRG neurons after MOG35-55 immunization.

Increased CXCL1 protein expression was also observed in primary cultured DRG neurons treated with MOG35-55, mediated by toll like receptor 4 (TLR4). TLR4 gene silencing or CXCL1 in DRG neurons was significantly attenuated neutrophil accumulation in the DRG and mechanical allodynia during the preclinical phase of EAE (around day 5 after immunization). Our results thus demonstrate that TLR4 pathway-CXCL1 in DRG neurons in DRG triggers neutrophil recruitment and subsequent mechanical allodynia in response to MOG35-55.

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