Here are a few studies on nicotine and MS
Novel Therapeutic Approach by Nicotine in Experimental Model of Multiple Sclerosis
...............Conclusion: Our data indicate that nicotine can significantly improve the clinical score and attenuate the demyelinating pathology typically found in experimental autoimmune encephalomyelitis, indicating that nicotine has protective effects in experimental model of multiple sclerosis.
Acta Pharmacologica Sinica - Nicotine and inflammatory neurological disorders
..............Epidemiological studies have shown an association of smoking with a higher occurrence of MS
35,
37,
39, while our results show that nicotine exposure significantly delays and attenuates inflammatory and autoimmune responses to myelin antigens in the mouse experimental autoimmune encephalomyelitis (EAE) model
40. This occurs whether nicotine treatment begins prior to, at the time of, or after immunization with myelin antigens to induce EAE. Moreover, nicotine exposure also suppresses disease development on adoptive transfer of autoimmune T cells. First, we demonstrated that the expansion of MOG-reactive T cells from the spleen in nicotine-treated mice was significantly dampened. In these animals, MOG-reactive Th cells produced less IFN-γ and IL-2 than cells from PBS-treated controls, whereas the production of IL-10, and particularly TGF-β, was augmented. A marginal, but not significant, reduction of IL-17 was observed in mice received nicotine. Our observation is somewhat surprising given the augmentation of TGF-β in nicotine exposed mice. Nicotine also did not appear to induce apoptosis in autoreactive T cells. This outcome invites the prediction that the immunological effects induced by nicotine may have contributed to the decreased T cell proliferation and altered cytokine profile. We also observed that, although the absolute numbers of CD4+CD25+ regulatory T cells were not dramatically altered by nicotine exposure, expression of FoxP3 was significantly upregulated. These regulatory T cells with enhanced FoxP3 expression may contribute to the suppression of T effector/autoreative cells. Furthermore, we found that nicotine significantly reduced levels of MHC class II, CD80, and CD86 expression on peripheral CD11c+ and CD11b+ cells. Notably, these changes were more dramatic for CD11b+ cells. It is likely that the altered APC phenotype in nicotine-treated animals may, at least in part, reduce the encephalitogenic capacity of MOG-reactive T cells in the EAE model.
In the CNS, in sharp contrast with control EAE mice, nicotine-treated animals had relatively few cellular infiltrates in CNS. Further, flow cytometry analysis of the cellular infiltrates showed that a significant reduction of CD4+, CD8+, CD19+, CD11c+, CD11b+, and CD11b+CD45+cell populations; and the reductions in CD19+ B cells and CD11c+ dendritic cells seem to reflect diminished migration into the CNS from the periphery. It is presently unclear whether the reduction of CD4+ and CD8+ cells in the CNS stems from reduced influx from the periphery, impaired expansion in the CNS after migration, or both. Whatever the mechanism may be, it is clear that there is significantly reduced expression of antigen presentation machinery by resident or infiltrating CD11c+and CD11b+ cells.
There are several possibilities as to how nicotine attenuates the disease even after EAE has been initiated after concurrence of CNS symptoms (
Table 2). Nicotine may inhibit myelin-reactive T cell determinant spreading when T cells migrating from the periphery encounter CNS antigens.........
Nicotine and serotonin in immune regulation and inflammatory processes: a perspective
