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NOX1/NADPH oxidase accelerates the onset of experimental arthritis

The critical role of phagocytic NOX2/NADPH oxidase in bacterial killing is well-known. However, the involvement of NOX1 isoform in immune responses has not been clarified. As NOX1 mRNA is expressed in such lymphoid tissues as spleen, thymus, bone marrow, and inguinal lymphoid nodes, we examined the role of NOX1 in experimental animal models using Nox1-deficient mice (Nox1-KO). When antibody production after ovalbumin (OVA) immunization was examined, no significant differences were observed in serum anti OVA IgG levels between wild-type mice (WT) and Nox1-KO. In the experimental asthma, the infiltration of eosinophils and the Th2 cytokine response after the induction of asthma with OVA were similar between the two genotypes. However, the severity and incidence of experimental collagen-induced arthritis (CIA) following the administration of a low dose of endotoxin (LPS) were significantly lower in Nox1-KO. While neither serum levels of autoantibodies nor in vitro cytokine responses following immunization with collagen were affected by Nox1 deficiency, NOX1 mRNA levels in the spleen significantly increased after the LPS challenge. Among the spleen cells, remarkable LPS-induced upregulation of NOX1 was demonstrated in both CD11b monocytes/macrophages and CD11c dendritic cells. The LPS-inducible NOX1 in monocytes/macrophages/dendritic cells may modulate the development of experimental CIA, providing a novel insight into the function of NOX1 in specific immune responses. Oral Sessions