MiR-155-5p facilitates acute lung injury progression via Th17 cells through the ETS-1/STAT3 pathway.

Acute lung injury (ALI) results from diverse intrapulmonary (direct) or extrapulmonary (indirect) factors, triggering a severe inflammatory response and resulting in varying degrees of damage to the intrapulmonary structures. Clinically, ALI often manifests as progressive hypoxic respiratory insufficiency with imaging changes in bilateral pulmonary infiltrates. ALI has a high mortality rate and poor prognosis among patients in the intensive care unit. The mechanism of ALI progression remains to be elucidated. The objective of the present research was to investigate how miR-155-5p affects T-helper (Th)17 cells in ALI and uncover the molecular mechanism involved. MiR-155-5p was found to be increased in ALI mice induced by lipopolysaccharide (LPS). Antagomir-miR-155-5p was used to suppress miR-155-5p expression, resulting in a positive outcome of alleviating lung damage and decreasing inflammation in ALI. The Th17 cell count in mouse lung tissue was reduced, as were levels of inflammatory markers such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, and IL-17. Our research showed that increased levels of miR-155-5p in ALI mice led to decreased ETS-1 levels and increased phosphorylation of STAT3. It looks like that antagomir-miR-155-5p suppressed Th17 cell production by inhibiting the above conditions, thereby attenuating ALI in mice. Agomir-miR-155-5p, however, observed the opposite result. MiR-155-5p appears to boost Th17 cell production and worsen inflammation in mice with LPS-induced ALI by suppressing ETS-1 expression and enhancing the STAT3 signaling pathway.