Nicotine modulates neurogenesis in the central canal during experimental autoimmune encephalomyelitis

Abstract

Nicotine has been shown to attenuate experimental autoimmune encephalomyelitis (EAE) through inhibiting inflammation in microglial populations during the disease course. In this study, we investigated whether nicotine modified the regenerative process in EAE by examining nestin-expressing neural stem cells (NSCs) in the spinal cord, which is the primary area of demyelination and inflammation in EAE. Our results show that the endogenous neurogenic responses in the spinal cord after EAE are limited and delayed: while nestin expression is increased, the proliferation of ependymal cells is inhibited compared to healthy animals. Nicotine application significantly reduced nestin expression and partially allowed for the proliferation of ependymal cells. We found that reduction of ependymal cell proliferation correlated with inflammation in the same area, which was relieved by administration of nicotine. Further, increased numbers of oligodendrocytes (OLs) were observed after nicotine treatment. These findings give a new insight into the mechanism of how nicotine functions to attenuate EAE.

A Western diet impairs CNS energy homeostasis and recovery after spinal cord injury: Link to astrocyte metabolism

“…In spinal cord gray matter by contrast, we observed increased Olig2+ OPCs in mice consuming HFHS at 14 and 30 dpi. Since prior studies have shown that the central canal region is a potential source of OPCs ( Gao et al, 2015 ), it is possible that the increase in Olig2+ OPCs in spinal cord gray matter after SCI, but the reduction in white matter, reflects an impairment in the migration of newly generated OPCs. Also, we cannot rule out any differential impact of HFHS on oligodendrocyte loss or proliferation across the gray and white matter after SCI ( Tripathi and McTigue, 2007 ; Vigano et al, 2013 ).…”

The Genetic Background of Mice Influences the Effects of Cigarette Smoke on Onset and Severity of Experimental Autoimmune Encephalomyelitis

“…Nicotine, one component of cigarettes, was attributed both pro- and anti-inflammatory effects on the immune system. Its signaling pathway [25,26,27] and cellular response has been investigated in several autoimmune diseases (for review [28]), including EAE [29,30]. The cholinergic system dampens the peripheral immune response indicating the involvement of the α7- nicotinic acetylcholine receptor (nAChR) [25,26], which is found both on neurons and the microglia.…”

Nicotine in Inflammatory Diseases: Anti-Inflammatory and Pro-Inflammatory Effects

“…Furthermore, 200 mg/ml nicotine hydrogen tartrate salt in drinking water induced mild, delayed, and chronic clinical signs and less inflammation in MOG 35-55 -induced female C57BL/6 mice (108). Nicotine (28 days, infusion rate of 0.25 ml/h, mini-osmotic pumps) was protective against experimental autoimmune encephalomyelitis by reducing nestin expression, partially allowing for the proliferation (Ki67 + ) of ependymal cells in areas of inflammation and increasing mature anti-inflammatory M2 subtype microglia (NG2 + and CC1 + ) to promote disease recovery (105,109). Nicotine also distinctively affected microglial viability, activation, and function, contrary to non-nicotine cigarette components, especially acrolein that has cytotoxic effects on microglia (105).…”