A small secreted protein triggers a TLR2/4-dependent inflammatory response during invasive Candida albicans infection
| العنوان: | A small secreted protein triggers a TLR2/4-dependent inflammatory response during invasive Candida albicans infection |
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| المؤلفون: | Zihou Deng, Longhai Tang, Wenjuan Wang, Chengshu Wang, Shuzhong Cui, Wencheng Zhu, Qun Zhao, Xiongjun Wang, Hui Xiao, Tiantian Li, Hongyu Wu, Jiangye Chen |
| المصدر: | Nature Communications, Vol 10, Iss 1, Pp 1-14 (2019) Nature Communications |
| بيانات النشر: | Nature Publishing Group, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | Male, 0301 basic medicine, Chemokine, General Physics and Astronomy, 02 engineering and technology, Mice, Candida albicans, lcsh:Science, Mice, Knockout, Multidisciplinary, biology, Toll-Like Receptors, Candidiasis, NF-kappa B, LIM Domain Proteins, 021001 nanoscience & nanotechnology, Corpus albicans, Cytokines, Chemokines, medicine.symptom, 0210 nano-technology, Science, Inflammation, Article, General Biochemistry, Genetics and Molecular Biology, Microbiology, Proinflammatory cytokine, 03 medical and health sciences, Immune system, medicine, Animals, Mitogen-Activated Protein Kinase Kinases, Innate immune system, General Chemistry, biochemical phenomena, metabolism, and nutrition, biology.organism_classification, Immunity, Innate, Toll-Like Receptor 2, Mice, Inbred C57BL, Toll-Like Receptor 4, Disease Models, Animal, TLR2, RAW 264.7 Cells, 030104 developmental biology, biology.protein, lcsh:Q, Carrier Proteins, Sequence Alignment |
| الوصف: | 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. The interplay between fungal pathogens and the innate immune system remains incompletely understood. Here, Wang et al. show that a small protein secreted by Candida albicans induces a TLR2- and TLR4-mediated inflammatory response in a mouse infection model. |
| اللغة: | English |
| تدمد: | 2041-1723 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::de5ee478139848ab715bcdc1726d4f8dTest http://link.springer.com/article/10.1038/s41467-019-08950-3Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....de5ee478139848ab715bcdc1726d4f8d |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 20411723 |
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