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

• Published in: Scientific reports Vol. 13; no. 1; p. 1293
• Main Authors: Cui, Xiao, Chen, Fangyan, Zhao, Jingya, Li, Dingchen, Hu, Mandong, Chen, Xue, Zhang, Yulin, Han, Li
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 23-01-2023; Nature Publishing Group; Nature Portfolio
• Subjects: 631/250; 631/326; 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
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-023-28567-3

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.