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This Article Full Text Full Text (PDF) Data Supplement All Versions of this Article: jimmunol.0901323v1 183/6/3578    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Joly, S. Articles by Sutterwala, F. S. PubMed PubMed Citation Articles by Joly, S. Articles by Sutterwala, F. S. Pubmed/NCBI databases Gene GEO Profiles HomoloGene Protein UniGene Substance via MeSH

Cutting Edge: Candida albicans Hyphae Formation Triggers Activation of the Nlrp3 Inflammasome¹

Sophie Joly^*,, Ning Ma, Jeffrey J. Sadler^*,, David R. Soll, Suzanne L. Cassel and Fayyaz S. Sutterwala^2,*,

^* Division of Infectious Diseases, Inflammation Program, and Division of Allergy and Immunology, Department of Internal Medicine and Department of Biology, University of Iowa, Iowa City, IA 52242

The proinflammatory cytokine IL-1β plays an important role in antifungal immunity; however, the mechanisms by which fungal pathogens trigger IL-1β 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-1β. 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- 1β 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 costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants K08 AI065517 (to F.S.S.) and K08 AI067736 (to S.L.C.).

² Address correspondence and reprint requests to Dr. Fayyaz S. Sutterwala, University of Iowa, 2501 Crosspark Road, D156 Multi-Tenant Facility, Coralville, IA 52241. E-mail address: fayyaz-sutterwala{at}uiowa.edu

³ Abbreviations used in this paper: WT, wild type; BMM, bone marrow macrophage; MOI, multiplicity of infection; M, macrophage.

⁴ The online version of this article contains supplemental material.