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Respiratory Syncytial Virus induces the classical ROS-dependent NETosis through PAD-4 and necroptosis pathways

Stéfanie P Muraro1, Gabriela F De Souza1, Stephanie W Gallo2

  • 1Laboratory of Clinical and Experimental Immunology, Infant Center, School of Medicine, Pontifical Catholic University of Rio Grande do Sul (PUCRS), Porto Alegre, RS, 90610-000, Brazil.

Scientific Reports
|September 23, 2018
PubMed

Insights

Respiratory syncytial virus (RSV) triggers neutrophils to release NETs, a key part of the immune response in young children. Understanding this NETosis pathway is crucial for developing new treatments for RSV bronchiolitis.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Respiratory syncytial virus (RSV) is a primary cause of infant bronchiolitis.
  • RSV infects pulmonary epithelial cells, initiating an immune response involving neutrophil recruitment.

Purpose of the Study:

  • To investigate the molecular mechanisms of Neutrophil Extracellular Trap (NET) production induced by RSV.

Main Methods:

  • Human neutrophils were stimulated with RSV to analyze NETosis.
  • Key signaling pathways (PI3K/AKT, ERK, p38 MAPK) and proteins (PAD-4, RIPK1, RIPK3, MLKL) were assessed.
  • RSV-infected epithelial cells and fibroblasts were used to evaluate neutrophil NET release.

Main Results:

  • RSV induced ROS-dependent NETosis, trapping the virus in DNA lattices with neutrophil elastase (NE) and myeloperoxidase (MPO).
  • NETosis signaling involved PI3K/AKT, ERK, p38 MAPK, PAD-4-mediated citrullination, and RIPK1/RIPK3/MLKL.
  • MLKL was essential for both NETosis and virus-induced neutrophil necrosis, leading to NET extrusion.
  • Neutrophils released NETs in response to RSV-infected alveolar epithelial cells and lung fibroblasts.

Conclusions:

  • RSV activates a complex signaling cascade leading to NETosis and necrosis in neutrophils.
  • Neutrophils recognize and respond to RSV-infected cells by releasing NETs.
  • Elucidating these mechanisms offers potential therapeutic targets for RSV-induced inflammation.

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