Neutrophils recruited to sites of infection protect from virus challenge by releasing neutrophil extracellular traps

Craig N. Jenne, Connie H.Y. Wong, Franz J. Zemp, Braedon McDonald, Masmudur M. Rahman, Peter A. Forsyth, Grant McFadden, Paul Kubes

Research output: Contribution to journalArticle

189 Scopus citations

Abstract

Neutrophils mediate bacterial clearance through various mechanisms, including the release of mesh-like DNA structures or neutrophil extracellular traps (NETs) that capture bacteria. Although neutrophils are also recruited to sites of viral infection, their role in antiviral innate immunity is less clear. We show that systemic administration of virus analogs or poxvirus infection induces neutrophil recruitment to the liver microvasculature and the release of NETs that protect host cells from virus infection. After systemic intravenous poxvirus challenge, mice exhibit thrombocytopenia and the recruitment of both neutrophils and platelets to the liver vasculature. Circulating platelets interact with, roll along, and adhere to the surface of adherent neutrophils, forming large, dynamic aggregates. These interactions facilitate the release of NETs within the liver vasculature that are able to protect host cells from poxvirus infection. These findings highlight the role of NETs and early tissue-wide responses in preventing viral infection.

Original languageEnglish (US)
Pages (from-to)169-180
Number of pages12
JournalCell Host and Microbe
Volume13
Issue number2
DOIs
StatePublished - Feb 13 2013

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Virology

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