The experimental autoimmune encephalomyelitis disease course is modulated by nicotine and other cigarette smoke components.

ABSTRACT: Epidemiological studies have reported that cigarette smoking increases the risk of developing multiple sclerosis (MS) and accelerates its progression. However, the molecular mechanisms underlying these effects remain unsettled. We have investigated here the effects of the nicotine and the non-nicotine components in cigarette smoke on MS using the experimental autoimmune encephalomyelitis (EAE) model, and have explored their underlying mechanism of action. Our results show that nicotine ameliorates the severity of EAE, as shown by reduced demyelination, increased body weight, and attenuated microglial activation. Nicotine administration after the development of EAE symptoms prevented further disease exacerbation, suggesting that it might be useful as an EAE/MS therapeutic. In contrast, the

SUBMITTER: Gao Z 

PROVIDER: S-EPMC4176721 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature