Ethanol modulates inflammatory responses of microglia

Alcohol consumption affects brain function, however its effects on brain's immune responses are poorly understood. Alcohol targets Ca‐activated K (BK) channels. Also, BK channels are activated during inflammation. Thus, ethanol may modify microglia inflammatory responses by targeting BK channels. We examined the effects of ethanol on LPS‐induced nitric oxide (NO) production by BV2 microglia as a measure of inflammatory response. We also investigated involvement of several K channels in inflammatory responses of BV2 cells. The cells were stimulated with LPS in the presence or absence of alcohol. NO levels were then measured in the media. Involvement of K channels was examined by including blockers of different K channels, among them TEA, apamin, and iberiotoxin. We also investigated if alcohol and K channels blockers affected activation of p38 MAPK, and NFκB. Ethanol exposure decreased NO production and p38 MAPK and NFκB activation in BV2 cells activated with LPS. NO production and activation of p38 and NFκB were down‐regulated by TEA and iberiotoxin in both control and ethanol‐treated cells. Apamin had no effect on NO production. This study shows that alcohol attenuates inflammatory responses of microglia, and K channels, in particular BK, but not SK channels are involved in these responses. However, alcohol does not appear to exert its anti‐inflammatory effects by targeting BK channels.