Sodium arsenite exposure impairs B cell proliferation and enhances vascular inflammation in Plasmodium berghei mouse model.

Abstract

Arsenic exposure has been linked to an impaired immune response and inflammation. Our study investigated the effects of sodium arsenite on host immune response and vascular inflammation during malarial infection. Mice were divided into three groups: control (C), Plasmodium berghei infection (I) and sodium arsenite exposure with Plasmodium berghei infection (As-I). The results showed that splenocyte proliferation stimulated by lipopolysaccharide (LPS) and pokeweed mitogen (PWM) was suppressed in the I group, and the suppression was more pronounced in the As-I group, suggesting that acquired immunity in infected mice was worsening following arsenic exposure. ICAM-1, an adhesion protein involved in parasite-infected red blood cell (iRBC) binding to endothelium, and HIF-1α, a hypoxia marker protein in the descending aorta, were increased in the As-I group compared to the I group. Collectively, our results suggest that arsenic may increase host susceptibility to malaria through suppression of B cell proliferation and enhancement of adhesion between iRBC and endothelium by increasing ICAM-1.