Sensory impairments and delayed regeneration of sensory axons in interleukin-6-deficient mice Academic Article uri icon

Overview

MeSH Major

  • Axons
  • Interleukin-6
  • Nerve Regeneration
  • Neurons, Afferent
  • Peripheral Nervous System
  • Sensation

abstract

  • 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.

publication date

  • June 1999

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed ID

  • 10341234

Additional Document Info

start page

  • 4305

end page

  • 13

volume

  • 19

number

  • 11