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Connective tissue diseases: Mitochondria drive NETosis and inflammation in SLE

Eric Boilard1, Paul R Fortin2

  • 1Department of Infectious Diseases and Immunity, Centre de Recherche du Centre Hospitalier Universitaire de Québec, Faculté de Médecine de l'Université Laval, 2705, Boulevard Laurier, Quebec City, Quebec G1V 4G2, Canada.

Nature Reviews. Rheumatology
|March 4, 2016
PubMed

Insights

Mitochondria released from cells can trigger inflammation. In lupus, mitochondrial respiration drives neutrophil extracellular trap formation, leading to inflammatory cytokine release.

Area of Science:

  • Cellular Biology
  • Immunology
  • Mitochondrial Research

Background:

  • Mitochondria, crucial for cellular energy via oxidative respiration, can also elicit inflammatory responses when released from cells, potentially due to their bacterial origins.
  • Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by chronic inflammation.

Discussion:

  • This study reveals a critical role for mitochondrial respiration in the formation of neutrophil extracellular traps (NETs) within the context of SLE.
  • Mitochondria extruded by neutrophils during NETosis are shown to be potent inducers of inflammatory cytokine production.

Key Insights:

  • Mitochondrial respiration is essential for NET formation in SLE.
  • Neutrophil-derived mitochondria actively promote inflammation by stimulating cytokine release.

Outlook:

  • Further investigation into targeting mitochondrial function in neutrophils could offer novel therapeutic strategies for SLE.
  • Understanding the precise mechanisms by which extracellular mitochondria activate inflammatory pathways is crucial for developing targeted immunomodulatory treatments.

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