Conclusion
Based on our analysis, we conclude that activating cGAS might increase host resistance to A. fumigatus, protect against pulmonary illnesses brought on by A. fumigatus and that exploring the cGAS-STING signaling pathway is beneficial not only for the immunological investigation of IPA but also may be a potential therapeutic objective.
Methods
An investigation into the infection of A. fumigatus was conducted by inhibiting cGAS activity in vivo and in vitro using siRNA and RU.521(an inhibitor of cGAS).
Results
We discovered that suppressing cGAS increased the host's susceptibility to A. fumigatus and harmed those with infections by enhancing pulmonary tissue damage and edema, as well as decreasing fungal clearance. Furthermore, our findings show that inhibiting or silencing cGAS can exacerbate the inflammatory response in IPA mouse models and human bronchi epithelial cells (HBECs) treated with A. fumigatus by upregulating the production of inflammatory genes with non-type 1 interferon.