Involvement of JNK signaling in Aspergillus fumigatus-induced inflammatory factors release in bronchial epithelial cells

Aspergillus fumigatus ( A. fumigatus ) is an important fungal pathogen and its conidia can be inhaled and interact with airway epithelial cells; however, the release of inflammatory factors from bronchial epithelial cells upon A. fumigatus infection and its regulation remained unclear. Here it was d...

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Bibliographic Details
Published in:Scientific reports 2023-01, Vol.13 (1), p.1293-1293, Article 1293
Main Authors: Cui, Xiao, Chen, Fangyan, Zhao, Jingya, Li, Dingchen, Hu, Mandong, Chen, Xue, Zhang, Yulin, Han, Li
Format: Article
Language:English
Subjects:
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Aspergillus fumigatus
Aspergillus fumigatus - metabolism
Autophagy
Conidia
Epithelial cells
Epithelial Cells - metabolism
Extracellular signal-regulated kinase
Humanities and Social Sciences
Inflammation
Interleukin 27
Interleukin-27 - metabolism
Kinases
MAP kinase
MAP Kinase Signaling System
Monocyte chemoattractant protein 1
multidisciplinary
Rapamycin
Science
Science (multidisciplinary)
Signal transduction
Tumor Necrosis Factor-alpha - metabolism
Tumor necrosis factor-α
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Summary:Aspergillus fumigatus ( A. fumigatus ) is an important fungal pathogen and its conidia can be inhaled and interact with airway epithelial cells; however, the release of inflammatory factors from bronchial epithelial cells upon A. fumigatus infection and its regulation remained unclear. Here it was demonstrated that the release of IL-27, MCP-1 and TNF-α from BEAS-2B cells were upregulated upon stimulation by conidia, while mitogen-activated protein kinase signaling pathway was activated. Further, the inhibition of JNK, but not p38 and ERK, could inhibit inflammatory factors release and the LC3II formation in BEAS-2B cells induced by A. fumigatus conidia. In addition, an inhibitor of autophagy, bafilomycin A1 was able to significantly down-regulate the release of inflammatory factors in BEAS-2B cells upon A. fumigatus conidia, while rapamycin could reverse the effect of JNK inhibitor on IL-27 and TNF-α release. Taken together, these data demonstrated that JNK signal might play an important role in inflammatory factor release regulated by autophagy in bronchial epithelial cells against A. fumigatus infection.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-023-28567-3