Role of PIM2 in acute lung injury induced by sepsis
- Juncai Ding
- Xiufang Yang
- Huijuan Huang
- Bo Wang
Affiliations: Department of Pediatrics, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, P.R. China, Department of Pediatrics, Zhongshan People's Hospital Affiliated to Sun Yat‑sen University, Zhongshan, Guangdong 528403, P.R. China, Department of Pediatrics, Zhongshan People's Hospital Affiliated to Sun Yat‑sen University, Zhongshan, Guangdong 528403, P.R. China, Department of Pediatrics, Guangdong Women and Children Hospital, Guangzhou, Guangdong 511442, P.R. China
- Published online on: June 30, 2022 https://doi.org/10.3892/etm.2022.11480
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Pediatric sepsis can cause lung damage leading to death in children. In addition, its complicated pathogenesis currently presents a difficult problem in the medical field. Proviral integrations of Moloney virus 2 (PIM2) is a prognostic marker of pediatric sepsis; therefore, the aim of the present study was to investigate the role of PIM2 in lung injury caused by pediatric sepsis. To meet this aim, the expression of PIM2 in lipopolysaccharide (LPS)‑induced BEAS‑2B pulmonary epithelial cells was detected using reverse transcription‑quantitative (RT‑q)PCR and western blotting. Subsequently, the expression of PIM2 was inhibited using the cell transfection technique. Cell Counting Kit‑8, TUNEL and western blotting, use of a fluorescence kit, ELISA detection kits were used to detect the expression of inflammatory‑ and cell injury‑associated indicators following PIM2 inhibition. In addition, the expression of proteins known to be associated with the Toll‑like receptor 2 (TLR2)/myeloid differentiation primary response 88 (MyD88) pathway were also assessed using western blotting. Finally, the simultaneous inhibition of PIM2 expression and overexpression of TLR2 were investigated in an attempt to elucidate the underlying mechanism. The expression level of PIM2 was revealed to be increased in LPS‑induced BEAS‑2B cells. Interference with PIM2 expression led to an increase in BEAS‑2B cell viability, the inhibition of apoptosis and a reduction in oxidative stress and the inflammatory response. These processes were also revealed to be accomplished via downregulation of the TLR2/MyD88 signaling pathway. Overall, the present study demonstrated that knockdown of PIM2 alleviated LPS‑induced bronchial epithelial cell injury by inhibiting the TLR2/MyD88 pathway.