tetano
Editor, Senior Moderator
Virology
. 2023 Jun 30;585:240-247.
doi: 10.1016/j.virol.2023.06.012. Online ahead of print. USP18 promotes innate immune responses and apoptosis in influenza A virus-infected A549 cells via cGAS-STING pathway
Li Tang[SUP] 1 [/SUP], Xi Liu[SUP] 1 [/SUP], Ce Wang[SUP] 1 [/SUP], Chang Shu[SUP] 2 [/SUP]
Affiliations
Influenza A virus (IAV) can infect respiratory epithelial cells where it replicates, triggers cellular innate immune responses, and even induces cell apoptosis. Ubiquitin-specific peptidase 18 (USP18) was reported to be associated with IAV replication and immune response homeostasis. Therefore, this study aimed to investigate the role of USP18 in IAV-infected lung epithelial cells. The cell viability was determined by the CCK-8 method. Viral titers were quantified by standard plaque assay. Innate immune response-associated cytokines were detected by RT-qPCR and ELISA and cell apoptosis was assessed by flow cytometry. The results showed that overexpression of USP18 promoted viral replication, innate immune factor secretion and apoptosis in IAV-infected A549 cells. Mechanistically, USP18 reduced cGAS degradation by decreasing its K48-linked ubiquitination to promote IAV-induced cGAS-STING pathway activation. In conclusion, USP18 is a pathological mediator of IAV in lung epithelial cells.
Keywords: Apoptosis; Influenza a virus; Innate immune; Mitochondria; USP18; cGAS-STING.
. 2023 Jun 30;585:240-247.
doi: 10.1016/j.virol.2023.06.012. Online ahead of print. USP18 promotes innate immune responses and apoptosis in influenza A virus-infected A549 cells via cGAS-STING pathway
Li Tang[SUP] 1 [/SUP], Xi Liu[SUP] 1 [/SUP], Ce Wang[SUP] 1 [/SUP], Chang Shu[SUP] 2 [/SUP]
Affiliations
- PMID: 37422930
- DOI: 10.1016/j.virol.2023.06.012
Influenza A virus (IAV) can infect respiratory epithelial cells where it replicates, triggers cellular innate immune responses, and even induces cell apoptosis. Ubiquitin-specific peptidase 18 (USP18) was reported to be associated with IAV replication and immune response homeostasis. Therefore, this study aimed to investigate the role of USP18 in IAV-infected lung epithelial cells. The cell viability was determined by the CCK-8 method. Viral titers were quantified by standard plaque assay. Innate immune response-associated cytokines were detected by RT-qPCR and ELISA and cell apoptosis was assessed by flow cytometry. The results showed that overexpression of USP18 promoted viral replication, innate immune factor secretion and apoptosis in IAV-infected A549 cells. Mechanistically, USP18 reduced cGAS degradation by decreasing its K48-linked ubiquitination to promote IAV-induced cGAS-STING pathway activation. In conclusion, USP18 is a pathological mediator of IAV in lung epithelial cells.
Keywords: Apoptosis; Influenza a virus; Innate immune; Mitochondria; USP18; cGAS-STING.