TRIM27 suppresses inflammation injuries in pediatric pneumonia by targeting TLR4/NF-κB signaling pathway

Shan Wang1, Baoxia Lu1, Jia Liu1

  • 1Department of Pediatric Ward Six, Lu'an People's Hospital, Luan Hospital Affiliated of Anhui Medical University, Lu'an, Anhui Province, China.

Insights

Tri-domain protein 27 (TRIM27) protects against pediatric pneumonia by reducing cell apoptosis and inflammation. TRIM27 inhibits the Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) pathway, offering a potential therapeutic target for pneumonia.

Area of Science:

  • Cellular and Molecular Biology
  • Immunology
  • Pediatric Medicine

Background:

  • Pediatric pneumonia is a significant global health concern with high morbidity and mortality.
  • Understanding pneumonia's mechanisms and identifying therapeutic targets are critical.
  • Tri-domain protein 27 (TRIM27), a member of the TRIM protein family, is involved in various cellular processes.

Purpose of the Study:

  • To investigate the protective role of TRIM27 in pediatric pneumonia.
  • To determine if TRIM27 expression influences cellular responses to inflammatory stimuli relevant to pneumonia.

Main Methods:

  • A lipopolysaccharide (LPS)-induced inflammation injury model in WI-38 cells was established.
  • TRIM27 expression levels were assessed in response to LPS.
  • The impact of TRIM27 on cell apoptosis and inflammatory responses was evaluated.
  • The involvement of the Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) pathway was analyzed.

Main Results:

  • LPS treatment downregulated TRIM27 expression in WI-38 cells.
  • Overexpression of TRIM27 reduced apoptosis and modulated inflammatory factors in LPS-treated cells.
  • TRIM27 overexpression inhibited the TLR4/NF-κB pathway, demonstrating an anti-inflammatory effect.

Conclusions:

  • TRIM27 exhibits a protective effect against LPS-induced inflammation in WI-38 cells.
  • TRIM27 exerts its anti-inflammatory action by inhibiting the TLR4/NF-κB signaling pathway.
  • TRIM27 represents a potential therapeutic target for pediatric pneumonia.
Abstract

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