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 demonstrated that the release of IL-27, MCP-1 and TNF-alpha 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-alpha 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.

Automated summary

The study found that the release of IL-27, MCP-1 and TNF-alpha from BEAS-2B cells was increased upon stimulation by A. fumigatus conidia, and the mitogen-activated protein kinase signaling pathway was activated. Furthermore, inhibition of JNK could suppress the release of inflammatory factors and LC3II formation in BEAS-2B cells induced by A. fumigatus conidia. Additionally, the autophagy inhibitor bafilomycin A1 significantly reduced the release of inflammatory factors, while rapamycin could reverse the effect of JNK inhibitor on IL-27 and TNF-alpha release. Overall, these findings suggest that JNK signaling may play an important role in autophagy-regulated inflammatory factor release in bronchial epithelial cells during A. fumigatus infection.