Journal
CURRENT MICROBIOLOGY
Volume 78, Issue 9, Pages 3474-3482Publisher
SPRINGER
DOI: 10.1007/s00284-021-02534-5
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Funding
- Chinese National Scientific Foundation [81273229, 81471565]
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The study demonstrates that swollen conidia of Aspergillus fumigatus induce the release of pro-inflammatory factors IL-8 and MCP-1 through activation of decrin-1 and CR3 receptors in lung epithelial A549 cells.
Invasive pulmonary aspergillosis induced by the pathogenic fungus Aspergillus fumigatus is one of the common fatal complications in immunocompromised patients. Lung epithelial cells play an important role in host immune defense against A. fumigatus. However, the interaction between lung epithelial cells and A. fumigatus conidia is not fully understood. In this study, we used the swollen conidia of A. fumigatus to stimulate the type II lung epithelial A549 cells. Results showed that swollen conidia could significantly increase RNA transcription and protein expression of interleukin 8 (IL-8) and monocyte chemoattractant protein 1 (MCP-1), but not TNF-alpha in A549 cells in a time-dependent manner. Moreover, serum opsonization was able to improve the release of inflammatory factors induced by swollen conidia. Blocking of the dectin-1 or CR3 receptors, or both simultaneously, in the A549 cells could decrease the release of IL-8 and MCP-1. Additionally, blocking dectin-1 or CR3 could inhibit the transcription of nuclear factor NF-kappa B that was activated by swollen conidia. Here we reported for the first time that dectin-1 and CR3 receptors in A549 cells mediate the release of pro-inflammatory factors IL-8 and MCP-1 induced by A. fumigatus.
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