Modulation of cytokine release from peripheral blood mononuclear cells from multiple sclerosis patients by coenzyme A and soraphen A

By applying the acetyl-CoA-carboxylase inhibitors soraphen A (SorA) and coenzyme A (CoA) ex vivo, we aimed to reduce proinflammatory cytokine release by PBMCs and increase anti-inflammatory cytokine levels, thereby demonstrating a possible application of those pathways in future multiple sclerosis (MS) therapy. In a prospective exploratory monocentric study, we analysed cytokine production by PBMCs treated with SorA (10 or 50 nM) and CoA (600 & mu;M). Thirty-one MS patients were compared to 18 healthy age-matched controls. We demonstrated the immunomodulatory potential of SorA and CoA in targeting the immune function of MS patients, with an overall reduction of cytokines except of IL-2, IL-6 and IL-10.

Automated summary

By using acetyl-CoA-carboxylase inhibitors Soraphen A (SorA) and coenzyme A (CoA) ex vivo, the study aimed to decrease the release of proinflammatory cytokines and increase anti-inflammatory cytokine levels in PBMCs, indicating a potential application in future multiple sclerosis (MS) therapy. The analysis of cytokine production in PBMCs treated with SorA (10 or 50 nM) and CoA (600μM) showed immunomodulatory effects in MS patients, with a reduction in cytokine levels overall except for IL-2, IL-6, and IL-10.