Journal
IMMUNOBIOLOGY
Volume 223, Issue 10, Pages 549-554Publisher
ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.imbio.2018.06.003
Keywords
Experimental autoimmune encephalomyelitis (EAE); IL-10; IL-17; S-Nitrosoglutathione (GSNO); T(H)1; T(H)17; Adoptive transfer
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Funding
- U.S. Department of Veterans Affairs [BX002829]
- National Institutes of Health [NS037766]
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In this study, we investigated IL-10 and IL-17 specific immunomodulatory potential of S-nitrosoglutathione (GSNO), a physiological nitric oxide carrier molecule, in experimental autoimmune encephalomyelitis (EAE). In active EAE model, GSNO treatment attenuated EAE severity and splenic CD4(+) T cells isolated from these mice exhibited decreased IL-17 expression without affecting the IFN-gamma expression compared to the cells from untreated EAE mice. Similarly, adoptive transfer of these cells to nave mice resulted in reduction in IL-17 expression in the spinal cords of recipient mice with milder EAE severity. CD4(+) T cells isolated from GSNO treated EAE mice, as compared to untreated EAE mice, still expressed lower levels of IL-17 under T(H)17 skewing conditions, but expressed similar levels of IFN-gamma under T(H)1 skewing condition. Interestingly, under both T(H)17 and T(H)1 skewing condition, CD4(+) T cells isolated from GSNO treated EAE mice, as compared to untreated EAE mice, expressed higher levels of IL-10 and adoptive transfer of these TH17 and TH1 skewed cells seemingly exhibited milder EAE disease. In addition, adoptive transfer of CD4(+) T cells from GSNO treated EAE mice to active EAE mice also ameliorated EAE disease with induction of spinal cord expression of IL-10 and reduction in of IL-17, thus suggesting the participation of IL-10 mechanism in GSNO mediated immunomodulation. GSNO treatment of mice passively immunized with CD4(+) T cells either from GSNO treated EAE mice or untreated mice further ameliorated EAE disease, supporting efficacy of GSNO for prophylaxis and therapy in EAR Overall, these data document a modulatory role of GSNO in IL-17/IL-10 axis of EAE and other autoimmune diseases.
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