LncRNA SNHG16 promotes LPS-induced human bronchial epithelial cell pyroptosis through miR-339-5p/NLRP1 axis mediation.

Introduction: Pyroptosis can aggravate lung injury in sepsis. It has been reported that lncRNA SNHG16 can regulate the inflammatory response. However, the role and underlying mechanism of SNHG16 in sepsis-induced pyroptosis and lung injury remain unclear.

Material and methods: To mimic septic lung injury in vitro, cells were treated with 1 µg/ml LPS. The Cell Counting Kit-8 (CCK-8) assay was performed to test cell viability. The lactate dehydrogenase (LDH) level was detected using a commercial kit. Interleukin (IL)-18 and IL-1 β secretion was tested using ELISA. Pyroptosis was investigated via flow cytometry. The relationship among SNHG16, miR-339-5p, and NLR family pyrin domain containing 1 (NLRP1) was explored using the dual luciferase assay.

Results: LPS significantly upregulated the levels of SNHG16 and NLRP1 in BEAS-2B cells. In addition, LPS significantly induced pyroptosis in BEAS2B cells, while this phenomenon was reversed by SNHG16 silencing. SNHG16 could bind with miR-339-5p, and NLRP1 was found to be the downstream mRNA of miR-339-5p. SNHG16 silencing significantly abolished the LPS-induced upregulation of NLRP1 through miR-339-5p downregulation. The upregulation of miR-339-5p inhibited the pro-apoptotic effect of LPS on BEAS-2B cells, which was abolished by NLRP1 overexpression. Furthermore, the anti-pyroptotic effect of SNHG16 siRNA was abolished by NLRP1 upregulation.

Conclusions: SNHG16 silencing reversed LPS-induced pyroptosis in BEAS-2B cells via miR-339-5p/NLRP1 axis mediation. Our study might shed new light on exploring therapeutic strategies for the treatment of septic lung injury.