Knocking down TNFAIP1 alleviates inflammation and oxidative stress in pediatric pneumonia through PI3K/Akt/Nrf2

Jing Chen1, Mengtian Zhao2, Wei Fang1

  • 1Department of Pediatric Cardiovascular Surgery, Anhui Provincial Children's Hospital, Hefei, Anhui, China.

Insights

Tumor necrosis factor alpha-inducible protein 1 (TNFAIP1) negatively regulates pneumonia by reducing inflammation and cell death. This protein may offer a new therapeutic target for treating acute respiratory infections in children.

Area of Science:

  • Immunology
  • Molecular Biology
  • Respiratory Medicine

Background:

  • Pneumonia is a significant global health concern, particularly affecting children.
  • Investigating the molecular mechanisms of childhood pneumonia is crucial due to increasing incidences.

Purpose of the Study:

  • To elucidate the role of tumor necrosis factor alpha-inducible protein 1 (TNFAIP1) in lipopolysaccharide (LPS)-induced pneumonia.
  • To analyze the involvement of the PI3K/Akt/Nrf2 pathway in TNFAIP1-mediated lung injury.

Main Methods:

  • LPS-induced pneumonia mouse model.
  • Assessment of lung function, TNFAIP1 expression, oxidative stress, apoptosis, and inflammation.
  • Western blot analysis to investigate the PI3K/Akt/Nrf2 signaling pathway.

Main Results:

  • TNFAIP1 expression was elevated in pneumonia but inversely correlated with lung injury.
  • Silencing TNFAIP1 reduced inflammation, reactive oxygen species (ROS), and apoptosis.
  • The PI3K/Akt/Nrf2 pathway was implicated in TNFAIP1's protective effects.

Conclusions:

  • TNFAIP1 acts as a negative regulator in acute pneumonia.
  • TNFAIP1 attenuates inflammation, ROS production, and apoptosis via the PI3K/Akt/Nrf2 pathway.
  • TNFAIP1 presents a potential therapeutic candidate for pneumonia treatment.
Abstract

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