白色念珠菌
单核细胞
吞噬作用
生物
糖皮质激素
肿瘤坏死因子α
地塞米松
白色体
内科学
内分泌学
微生物学
免疫学
医学
作者
Stefan Heidenreich,Tobias Kubis,Michael Schmidt,W. Fegeler
标识
DOI:10.1006/cimm.1994.1230
摘要
The mechanisms of glucocorticoid-induced immunosuppression of human monocytes for the defense of Candida albicans were examined in this in vitro study. Dexamethasone at pharmacological concentrations (10-7-10-5M) dose-dependently attenuated growth inhibition of C. albicans by resident monocytes. In interferon-γ (IFN-γ)-primed monocytes, fungal growth inhibition was maximal and not altered by dexamethasone. Similarly, phagocytosis and killing of Candida by monocytes were not affected by steroids. To study the underlying mechanisms, we found that Candida-induced synthesis of tumor necrosis factor-α (TNF-α) by monocytes was completely abrogated by dexamethasone. Substitution of TNF-α to dexamethasone-treated monocytes fully reversed the alterations of growth inhibition of C. albicans induced by steroids. These findings suggest that glucocorticoids affect the growth control of Candida by monocytes indirectly via suppression of the formation of TNF-α, which is required as an autocrine cofactor for full monocyte activation.
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