ATG16L1 regulated IL-22 induced IFN level in Pseudomonas aeruginosa Lung Infection via cGAS signal passage.

Objective: This study explored that the possible effects and mechanism of ATG16L1 in pseudomonas aeruginosa lung infection.

Methods: C57BL/6J mice were anesthetized with isoflurane and intratracheally (I.T.) inoculated with 5 × 106 CFU of Pseudomonas aeruginosa strain PA14. RAW264.7 macrophages were stimulated with 0.1 mg/ml of lipopolysaccharide (LPS). RAW264.7 macrophages were stimulated with 0.1 mg/ml LPS. Hematoxylin-Eosin (H&E), Immunofluorescence, sample acquisition, qPCR validation, Enzyme linked immunosorbent assay (ELISA) and immunofluorescence analysis were used this experiment.

Results: ATG16L1 mRNA and protein expressions in mice with pseudomonas aeruginosa lung infection were also suppressed. ATG16L1 gene reduced inflammation and INF-γ levels in vitro model. On the other hand, ATG16L1 protein presented lung injury and inflammation levels in mice of pseudomonas aeruginosa lung infection. ATG16L1 regulated cGAS/IL-22 signal passage in model of pseudomonas aeruginosa lung onfection.

Conclusion: These findings indicate that ATG16L1 reduced IL-22 induced IFN level in pseudomonas aeruginosa lung infection via cGAS signal passage, which may provide a new therapeutic scheme for viral diseases or inflammatory diseases and its associated complications.