LncRNA NR_003508 Boosts Pseudomonas aeruginosa-Induced Autophagy by Facilitating the Conversion of LC3-I to LC3-II and p62 Degradation.

LncRNA NR_003508 has been implicated in lipopolysaccharide (LPS)-induced acute respiratory distress syndrome. Yet, the involvement of LncRNA NR_003508 in Pseudomonas aeruginosa (PA)-induced autophagy remains elusive. This study aims to reveal the underlying mechanisms of LncRNA NR_003508 in PA-induced autophagy, thereby enhancing the basic research content of the pathogenesis of PA infection. Fluorescence in situ hybridization (FISH) probes and q-PCR revealed that PA infection induced macrophage autophagy accompanied by increasing LncRNA NR_003508, suggesting that LncRNA NR_003508 may participate in competing endogenous RNA (ceRNA)-mediated regulatory networks. Concurrently, autophagic clearance of PA requires LncRNA NR_003508. Then, we used the Gene Expression Omnibus (GEO) database to find that LC3 was considered a core protein in PA-infected autophagy. Furthermore, LncRNA NR_003508 promoted the formation of autophagosomes, which played a positive role in PA clearance. Functionally, bioinformatics analysis and luciferase reporter assays demonstrated that LncRNA NR_003508 promotes the conversion of LC3I to LC3II by sponging miR-344i and facilitates p62 degradation by binding to miR-344g-5p. Taken together, our data established that LncRNA NR_003508 enhanced the formation of autophagosomes induced by PA infection via the miR-344i/LC3 and miR-344g-5p/p62 axes, partly boosting the clearance of PA and providing a theoretical basis and experimental support for understanding the mechanisms underlying PA infection.