Premium
Nitric oxide plays a key role in the platelet‐activating factor‐induced enhancement of resistance against systemic candidiasis
Author(s) -
Kim HanA,
Kim SoHee,
Ko HyunMi,
Choi JungHwa,
Kim KyoungJin,
Oh SinHye,
Cho KyoungOh,
Choi IlWhan,
Im SuhnYoung
Publication year - 2008
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2007.02795.x
Subject(s) - platelet activating factor , nitric oxide , candida albicans , chemokine , nitric oxide synthase , corpus albicans , cxc chemokine receptors , microbiology and biotechnology , messenger rna , chemistry , biology , pharmacology , immunology , inflammation , endocrinology , biochemistry , chemokine receptor , gene
Summary Platelet‐activating factor (PAF) has been demonstrated to augment resistance against Candida albicans infection. In this study, the role of nitric oxide (NO) in PAF‐induced resistance in the kidneys was investigated. Pretreatment of the C. albicans ‐infected mice with PAF resulted in strong expression of messenger RNA (mRNA) and the protein synthesis of inducible nitric oxide synthase (iNOS). These PAF effects were inhibited to a significant degree by pretreatment with the nuclear factor‐κB inhibitor, pyrrolidinedithiocarbamate. Pretreatment with PAF protected the mice from death caused by C. albicans infection and reduced the growth of fungus in the kidneys. The protective activity of PAF was abrogated by pretreatment with the iNOS inhibitor, aminoguanidine, and in the iNOS −/− mice. The PAF markedly increased the infiltration of neutrophils, but not macrophages, and also enhanced the mRNA expression levels of the CXC chemokine, keratinocyte‐derived chemokine, in C. albicans ‐infected kidneys. These effects of PAF were attenuated in the aminoguanidine‐treated mice and the iNOS −/− mice. These data show that NO plays an important role in PAF‐induced protection against C. albicans .