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.