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Role of PIM2 in acute lung injury induced by sepsis

Juncai Ding1,2, Xiufang Yang2, Huijuan Huang2

  • 1Department of Pediatrics, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, P.R. China.

Experimental and Therapeutic Medicine
|August 18, 2022
PubMed

Insights

Proviral integrations of Moloney virus 2 (PIM2) protects against lung injury in pediatric sepsis by downregulating the Toll-like receptor 2/myeloid differentiation primary response 88 pathway. This finding offers a new therapeutic target for treating pediatric sepsis-induced lung damage.

Area of Science:

  • Pulmonary Medicine
  • Molecular Biology
  • Immunology

Background:

  • Pediatric sepsis can lead to severe lung damage and mortality.
  • The complex pathogenesis of pediatric sepsis presents significant clinical challenges.
  • Proviral integrations of Moloney virus 2 (PIM2) has been identified as a prognostic marker in pediatric sepsis.

Purpose of the Study:

  • To investigate the role of PIM2 in pediatric sepsis-induced lung injury.
  • To explore the underlying molecular mechanisms involving PIM2 in lung epithelial cells.

Main Methods:

  • Lipopolysaccharide (LPS)-induced BEAS-2B pulmonary epithelial cells were used.
  • PIM2 expression was detected using RT-qPCR and western blotting.
  • PIM2 was inhibited via cell transfection, and subsequent effects on cell viability, apoptosis, oxidative stress, and inflammation were assessed.
  • The Toll-like receptor 2 (TLR2)/myeloid differentiation primary response 88 (MyD88) pathway was analyzed.

Main Results:

  • PIM2 expression was upregulated in LPS-induced BEAS-2B cells.
  • Inhibition of PIM2 increased cell viability, reduced apoptosis, and decreased oxidative stress and inflammation.
  • These protective effects were associated with the downregulation of the TLR2/MyD88 signaling pathway.

Conclusions:

  • Knockdown of PIM2 alleviates lung injury in a model of pediatric sepsis.
  • PIM2 inhibition protects bronchial epithelial cells by suppressing the TLR2/MyD88 pathway.
  • Targeting PIM2 may represent a novel therapeutic strategy for pediatric sepsis-induced lung injury.

Keywords:
Toll-like receptor 2/myeloid differentiation primary response 88 pathwaycell injurypediatric sepsisproviral integrations of Moloney virus 2

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