The immune response of upper and lower airway epithelial cells to Aspergillus fumigatus and Candida albicans-derived β-glucan in Th17 type cytokine environment
Murat Turkbey, Dilara Karaguzel, Ali Doruk Uzunkaya, Yusuf Doruk Aracagok, Cagatay Karaaslan
{"title":"The immune response of upper and lower airway epithelial cells to Aspergillus fumigatus and Candida albicans-derived β-glucan in Th17 type cytokine environment","authors":"Murat Turkbey, Dilara Karaguzel, Ali Doruk Uzunkaya, Yusuf Doruk Aracagok, Cagatay Karaaslan","doi":"10.1007/s00203-025-04266-7","DOIUrl":null,"url":null,"abstract":"<div><p>The fungal cell wall component β-glucan activates inflammation via the Dectin-1 receptor and IL-17 coordinates the antifungal immunity. However, the molecular crosstalk between IL-17, Dectin-1, and β-glucan in epithelial cells and fungal immunity remains unclear. We investigated the impact of <i>A.fumigatus</i>-derived β-glucan (AFBG) and <i>C.albicans</i>-derived β-glucan (CABG) on Dectin-1 and cytokines in nasal epithelial cells (NECs) and bronchial epithelial cells (BECs) in the presence of IL-17. CABG reduced BEC viability more than AFBG despite similar Dectin-1 expression. IL-17 reduced β-glucan-dependent Dectin-1 expression in NECs but increased it in BECs after 12 h. AFBG synergized with IL-17, enhancing pro-inflammatory cytokines and chemokine expressions. IL-6 and IL-8 production increased in the presence of IL-17. Th17 cytokine influenced the Dectin-1 response to fungal β-glucan in NECs and BECs, impacting the initiation and nature of epithelial cell reactions to AFBG and CABG. Uncovering the molecular mechanisms of fungal β-glucans in the respiratory tract could lead to novel strategies for preventing fungal diseases.</p></div>","PeriodicalId":8279,"journal":{"name":"Archives of Microbiology","volume":"207 4","pages":""},"PeriodicalIF":2.3000,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archives of Microbiology","FirstCategoryId":"99","ListUrlMain":"https://link.springer.com/article/10.1007/s00203-025-04266-7","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
The fungal cell wall component β-glucan activates inflammation via the Dectin-1 receptor and IL-17 coordinates the antifungal immunity. However, the molecular crosstalk between IL-17, Dectin-1, and β-glucan in epithelial cells and fungal immunity remains unclear. We investigated the impact of A.fumigatus-derived β-glucan (AFBG) and C.albicans-derived β-glucan (CABG) on Dectin-1 and cytokines in nasal epithelial cells (NECs) and bronchial epithelial cells (BECs) in the presence of IL-17. CABG reduced BEC viability more than AFBG despite similar Dectin-1 expression. IL-17 reduced β-glucan-dependent Dectin-1 expression in NECs but increased it in BECs after 12 h. AFBG synergized with IL-17, enhancing pro-inflammatory cytokines and chemokine expressions. IL-6 and IL-8 production increased in the presence of IL-17. Th17 cytokine influenced the Dectin-1 response to fungal β-glucan in NECs and BECs, impacting the initiation and nature of epithelial cell reactions to AFBG and CABG. Uncovering the molecular mechanisms of fungal β-glucans in the respiratory tract could lead to novel strategies for preventing fungal diseases.
期刊介绍:
Research papers must make a significant and original contribution to
microbiology and be of interest to a broad readership. The results of any
experimental approach that meets these objectives are welcome, particularly
biochemical, molecular genetic, physiological, and/or physical investigations into
microbial cells and their interactions with their environments, including their eukaryotic hosts.
Mini-reviews in areas of special topical interest and papers on medical microbiology, ecology and systematics, including description of novel taxa, are also published.
Theoretical papers and those that report on the analysis or ''mining'' of data are
acceptable in principle if new information, interpretations, or hypotheses
emerge.