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Park7 interacts with p47(phox) to direct NADPH oxidase-dependent ROS production and protect against sepsis

Wenjun Liu1, Hailong Wu1, Lili Chen1

  • 1State Key Laboratory for Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China.

Cell Research
|May 30, 2015
PubMed

Insights

Parkinson disease 7 (Park7) protects against sepsis by regulating inflammation and macrophage function. Loss of Park7 increases sepsis mortality by impairing reactive oxygen species production and bacterial clearance.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Sepsis mortality is linked to inappropriate inflammatory responses.
  • Reactive oxygen species (ROS), produced by NADPH oxidase via Toll-like receptors (TLRs), modulate inflammation.
  • Parkinson disease 7 (Park7) is known for its role in eliminating ROS.

Purpose of the Study:

  • To investigate the role of Park7 in modulating inflammation and mortality during sepsis.
  • To elucidate the mechanism by which Park7 influences sepsis outcomes.

Main Methods:

  • Utilized a murine model of sepsis, comparing wild-type and Park7(-/-) mice.
  • Assessed mortality, bacterial burden, systemic and local inflammation markers.
  • Investigated macrophage phagocytosis, bacterial killing, ROS production, and cytokine profiles.
  • Examined the interaction between Park7 and p47(phox) using cellular assays.

Main Results:

  • Park7(-/-) mice exhibited significantly higher mortality and bacterial loads in sepsis.
  • Park7 deficiency led to decreased systemic and local inflammation, impaired macrophage phagocytosis, and reduced bacterial killing.
  • Park7-deficient macrophages failed to produce ROS and proinflammatory cytokines upon stimulation.
  • Park7 directly binds to p47(phox) to promote NADPH oxidase-dependent ROS production.
  • Restoring Park7 expression rescued ROS production and improved survival in LPS-induced sepsis.

Conclusions:

  • Park7 plays a critical protective role in sepsis.
  • Park7 controls sepsis outcomes by regulating macrophage activation, NADPH oxidase activity, and inflammatory responses through ROS production.

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