Stimulation of cholinergic anti-inflammatory system by nicotine alleviates autoimmune encephalomyelitis through immune responses change

Recently, it has demonstrated that the signaling by the α7 nicotinic receptors produces the anti-inflammatory condition in both macrophages and T cells. Moreover, activation of macrophages and T cells have a very important role in multiple sclerosis (MS). In the present study, the therapeutic effect of nicotine, on experimental autoimmune encephalomyelitis (EAE), an animal model of MS, and its effects on T-helper cells responses have been evaluated.
In this experimental study, EAE was induced by guinea pig spinal cord homogenate and complete Freund’s adjuvant in wistar rats. Animals were allocated in two therapeutic groups (n=7 per group). Treatment with nicotine (2.5 mg/kg-daily) was started in treatment group when the treatment group developed a disability score (at day 12). EAE control received vehicle alone with the same schedule. Signs of disease were recorded daily until the day 36 when animals were sacrificed. The Splenocytes were checked for proliferation by MTT test and cytokine production by ELISA. The level of nitric oxide in serum was checked by griess test. The clinical scores were analyzed by Mann Whitney-U and the other data were analyzed by Student’s t-test
Nicotine administration after the occurrence of clinical symptoms significantly regressed the clinical features of EAE. Alongside with the decrease in nitric oxide, nicotine significantly inhibited the production of pro-inflammatory IL-17 as well as IFN-γ. The levels of anti-inflammatory IL-10 were not altered significantly. Lymphocyte proliferation was significantly decreased in treatment group compared to control group.
The results of this study show that nicotine has immunomodulatory benefits and can be used for control of MS disease.