| Abstrakt: |
Candida albicans is a leading cause of invasive candidiasis. C. albicans NBRC 1385 releases a mannoprotein beta-glucan complex (CAWS) into C-limiting medium. CAWS induced various biological activities, such as cytokine synthesis by leukocytes, platelet aggregation, acute lethal toxicity, induction of coronary arteritis, and the enhancement of side effects of indomethacin. CAWS is a ligand for dectin-2 and functions as pathogen associated molecular patterns (PAMPS). CAWS induced coronary arteritis (CAWS vasculitis) resembling that seen in patients with Kawasaki disease (KD). CAWS vasculitis has been applied to clarify the molecular mechanisms and to develop therapeutic strategies for KD. Detoxification of PAMPS gradually proceeds in the host by binding proteins, neutrophils, and macrophages and is the limiting factor to defme the time course of acute as well as chronic inflammatory diseases. To clarify the detoxification of CAWS by oxidative stress, CAWS were treated with NaOH, H2SO4, or sodium hypochlorite and tested for the modification of the structure, acute lethal toxicity and CAWS vasculitis. It was found that the structure and function of CAWS was stable with 1.0 N NaOH, 1.0 N H2SO4, or 2% sodium hypochlorite treatment. These data strongly suggest that the structure of CAWS is essential to induce pathological activities of Candida, and are resistant to oxidative detoxification stress in the host. [ABSTRACT FROM AUTHOR] |
