A small secreted protein triggers a TLR2/4-dependent inflammatory response during invasive Candida albicans infection

Wenjuan Wang, Zihou Deng, Hongyu Wu, Qun Zhao, Tiantian Li, Wencheng Zhu, Xiongjun Wang, Longhai Tang, Chengshu Wang, Shu-Zhong Cui, Hui Xiao () and Jiangye Chen ()
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Wenjuan Wang: Chinese Academy of Sciences
Zihou Deng: Chinese Academy of Sciences
Hongyu Wu: Chinese Academy of Sciences
Qun Zhao: Chinese Academy of Sciences
Tiantian Li: Chinese Academy of Sciences
Wencheng Zhu: Chinese Academy of Sciences
Xiongjun Wang: Chinese Academy of Sciences
Longhai Tang: Suzhou Blood Center
Chengshu Wang: Chinese Academy of Sciences
Shu-Zhong Cui: Guangzhou Medical University
Hui Xiao: Chinese Academy of Sciences
Jiangye Chen: Chinese Academy of Sciences

Nature Communications, 2019, vol. 10, issue 1, 1-14

Abstract: Abstract Candida albicans can switch from commensal to pathogenic mode, causing mucosal or disseminated candidiasis. The host relies on pattern-recognition receptors including Toll-like receptors (TLRs) and C-type lectin receptors (CLRs) to sense invading fungal pathogens and launch immune defense mechanisms. However, the complex interplay between fungus and host innate immunity remains incompletely understood. Here we report that C. albicans upregulates expression of a small secreted cysteine-rich protein Sel1 upon encountering limited nitrogen and abundant serum. Sel1 activates NF-κB and MAPK signaling pathways, leading to expression of proinflammatory cytokines and chemokines. Comprehensive genetic and biochemical analyses reveal both TLR2 and TLR4 are required for the recognition of Sel1. Further, SEL1-deficient C. albicans display an impaired immune response in vivo, causing increased morbidity and mortality in a bloodstream infection model. We identify a critical component in the Candida-host interaction that opens a new avenue to tackle Candida infection and inflammation.

Date: 2019
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DOI: 10.1038/s41467-019-08950-3

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