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Interleukin-6 (IL-6) is a multifunctional cytokine mediating inflammatory or immune reactions. Here we investigated the possible role of IL-6 in the intact or lesioned peripheral nervous system using adult IL-6 gene knockout (IL-6−/−) mice. Various sensory functions were tested by applying electrophysiological, morphological, biochemical, and behavioral methods. There was a 60% reduction of the compound action potential of the sensory branch of IL-6−/− mice as compared with the motor branch in the intact sciatic nerve. Cross sections of L5 DRG of IL-6−/− mice showed a shift in the relative size distribution of the neurons. The temperature sensitivity of IL-6−/− mice was also significantly reduced. After crush lesion of the sciatic nerve, its functional recovery was delayed in IL-6−/− mice as analyzed from a behavioral footprint assay. Measurements of compound action potentials 20 d after crush lesion showed that there was a very low level of recovery of the sensory but not of the motor branch of IL-6−/− mice. Similar results of sensory impairments were obtained with mice showing slow Wallerian degeneration (Wlds) and a delayed lesion-induced recruitment of macrophages. However, in contrast to WldS mice, in IL-6−/− mice we observed the characteristic lesion-induced invasion of macrophages and the upregulation of low-affinity neurotrophin receptor p75 (p75LNTR) mRNA levels identical to those of IL-6+/+ mice. Thus, the mechanisms leading to the common sensory deficiencies were different between IL-6−/− and WldS mice. Altogether, the results suggest that interleukin-6 is essential to modulate sensory functions in vivo.

Sensory Impairments and Delayed Regeneration of Sensory Axons in Interleukin-6-Deficient Mice