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

Involvement of JNK signaling in Aspergillus fumigatus-induced inflammatory factors release in bronchial epithelial cells.
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JNK信号参与烟曲霉诱导支气管上皮细胞炎症因子释放

DOI:
10.1038/s41598-023-28567-3
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发表时间:
2023-01-23
期刊:
影响因子:
4.6
通讯作者:
--
中科院分区:
综合性期刊3区
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--
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烟曲霉菌是一种重要的真菌病原菌,其分生孢子可被吸入并与呼吸道上皮细胞相互作用,但其呼吸道上皮细胞释放炎症因子对烟曲霉菌感染的影响及其调控机制尚不清楚。结果表明,分生孢子刺激BEAS-2B细胞释放IL-27、单核细胞趋化蛋白-1和肿瘤坏死因子-α,激活了丝裂原活化蛋白激酶信号转导通路。此外,抑制JNK,而不是抑制p38和ERK,可以抑制烟曲霉分生孢子诱导的BEAS-2B细胞中炎症因子的释放和LC_3II的形成。此外,自噬抑制剂巴菲霉素A1能显著下调BEAS-2B细胞对烟曲霉分生孢子炎性因子的释放,而雷帕霉素则能逆转JNK抑制剂对IL-27和肿瘤坏死因子-α释放的影响。综上所述,这些数据表明,JNK信号可能在自噬调节的炎症因子释放中发挥重要作用。
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.
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