| First Author | Chisholm SP | Year | 2012 |
| Journal | J Neurosci | Volume | 32 |
| Issue | 4 | Pages | 1146-55 |
| PubMed ID | 22279201 | Mgi Jnum | J:180507 |
| Mgi Id | MGI:5306513 | Doi | 10.1523/JNEUROSCI.5343-11.2012 |
| Citation | Chisholm SP, et al. (2012) Interleukin-17A Increases Neurite Outgrowth from Adult Postganglionic Sympathetic Neurons. J Neurosci 32(4):1146-55 |
| abstractText | Inflammation can profoundly alter the structure and function of the nervous system. Interleukin (IL)-17 has been implicated in the pathogenesis of several inflammatory diseases associated with nervous system plasticity. However, the effects of IL-17 on the nervous system remain unexplored. Cell and explant culture techniques, immunohistochemistry, electrophysiology, and Ca(2+) imaging were used to examine the impact of IL-17 on adult mouse sympathetic neurons. Receptors for IL-17 were present on postganglionic neurons from superior mesenteric ganglia (SMG). Supernatant from activated splenic T lymphocytes, which was abundant in IL-17, dramatically enhanced axonal length of SMG neurons. Importantly, IL-17-neutralizing antiserum abrogated the neurotrophic effect of splenocyte supernatant, and incubation of SMG neurons in IL-17 (1 ng/ml) significantly potentiated neurite outgrowth. The neurotrophic effect of IL-17 was accompanied by inhibition of voltage-dependent Ca(2+) influx and was recapitulated by incubation of neurons in a blocker of N-type Ca(2+) channels (omega-conotoxin GVIA; 30 nm). IL-17-induced neurite outgrowth in vitro appeared to be independent of glia, as treatment with a glial toxin (AraC; 5 mum) did not affect the outgrowth response to IL-17. Moreover, application of the cytokine to distal axons devoid of glial processes enhanced neurite extension. An inhibitor of the NF-kappaB pathway (SC-514; 20 mum) blocked the effects of IL-17. These data represent the first evidence that IL-17 can act on sympathetic somata and distal neurites to enhance neurite outgrowth, and identify a novel potential role for IL-17 in the neuroanatomical plasticity that accompanies inflammation. |
