NITRIC-OXIDE ENHANCES RESISTANCE OF SCID MICE TO MUCOSAL CANDIDIASIS

The capacity of macrophages from SCID and C.B-17 mice to kill Candida albicans via a nitric oxide (NO)-dependent pathway and the contributio n of NO in resistance to mucosal candidiasis were assessed. In vitro, an inhibitor of NO synthase (NOS) reduced the candidacidal activity an d nitrite-producing capacity of activated resident peritoneal macropha ges from immunocompetent C.B-17 and immunodeficient SCID mice. In vivo , stomachs from gnotobiotic SCID mice that were colonized with a pure culture of C. albicans had low-grade infections and expressed inducibl e NOS (iNOS) mRNA. C. albicans-monoassociated SCID mice treated with a n inhibitor of NOS had more severe orogastric candidiasis than control s. These data suggest that NO contributes to the candidacidal capacity of activated macrophages from C.B-17 and SCID mice and that NO synthe sized by iNOS may contribute to the resistance of SCID mice to mucosal candidiasis.