Cutting Edge: Candida albicans Hyphae Formation Triggers Activation of the NlrP3 Inflammasome

被引：233

作者：

Joly, Sophie ^{[1
,2
]}

Ma, Ning ^{[4
]}

Sadler, Jeffrey J. ^{[1
,2
]}

Soll, David R. ^{[4
]}

Cassel, Suzanne L. ^{[3
]}

Sutterwala, Fayyaz S. ^{[1
,2
]}

机构：

[1] Univ Iowa, Div Infect Dis, Iowa City, IA 52242 USA

[2] Univ Iowa, Inflammat Program, Iowa City, IA 52242 USA

[3] Univ Iowa, Dept Internal Med, Div Allergy & Immunol, Iowa City, IA 52242 USA

[4] Univ Iowa, Dept Biol, Iowa City, IA 52242 USA

来源：

JOURNAL OF IMMUNOLOGY | 2009年 / 183卷 / 06期

基金：

美国国家卫生研究院;

关键词：

FINGERPRINTING PROBES; ADAPTIVE IMMUNITY; DENDRITIC CELLS; HOST-DEFENSE; IN-VIVO; PATHOGENS; CASPASE-1; GLABRATA; INNATE;

D O I：

10.4049/jimmunol.0901323

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The proinflammatory cytokine IL-1 beta plays an important role in antifungal immunity;, however, the mechanisms by which fungal pathogens trigger IL-1 beta secretion are unclear. In this study we show that infection with Candida albicans is sensed by the Nlrp3 inflammasome, resulting in the subsequent release of IL-1 beta. The ability of C. albicans to switch from a unicellular yeast form into a filamentous form is essential for activation of the Nlrp3 inflammasome, as C. albicans mutants incapable of forming hyphae were defective in their ability to induce macrophage IL-1 beta secretion. Nlrp3-deficient mice also demonstrated increased susceptibility to infection with C. albicans, which is consistent with a key role for Nlrp3 in innate immune responses to the pathogen C. albicans. The Journal of Immunology, 2009, 183: 3578-3581.

引用

页码：3578 / 3581

页数：4

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