Neutrophils Recruited to Sites of Infection Protect from Virus Challenge by Releasing Neutrophil Extracellular Traps

Craig N. Jenne et al. Cell Host Microbe 2013; 13(2):169-80

Speaker: Pei-Wei Chen (陳珮瑋)                                          Time: 14:10~15:00, Apr. 10, 2013

Commentator: Dr. Chung-Hsin Tseng (曾忠信 老師)        Place: Room 601

Abstract:

Neutrophils are the first immune cells to the site of injury and microbial infection. Recently, a novel antimicrobial mechanism of neutrophils has been described, in which neutrophils release decondensed chromatin from their nuclei and result in the generation of a net-like structure calledneutrophil extracellular traps (NETs). These NETs are covered with proteases and other antimicrobial molecules that bind and kill microorganisms⁽¹⁾. Neutrophils are crucial players in controlling bacterial and fungal infections, while the role of NETs in the host antiviral response is still unclear. The authors systemically treated mice with viral analogs and myxoma virus, and found these treatments induce neutrophil recruitment to the liver microvasculature. They also found Kupffer cells and the adhesion molecule CD11b play important roles in inducing neutrophil recruitment after viral challenge. Previous studies have demonstrated that the release of NETs can be induced by platelets binding to adherent neutrophils in blood vessels⁽²⁾. The authors further observed massive platelet sequestration within the liver after viral challenge. Moreover, the attenuation of platelet aggregation decreased NET formation. The results indicate that platelet accumulation on the adherent neutrophils is essential for NET generation. Most importantly, the authors demonstrated that viral infection induces the production of NETs, which protect host cells from disseminating viral infection. In conclusion, this study shows a dynamic and coordinated innate immune response to systemic viral challenge that involves the recruitment of neutrophils and platelets to the liver. The production of intravascular NETs provides the protection for host cells against viral infection in vivo.

References:

1.      Phillipson M, Kubes P. The neutrophil in vascular inflammation. Nature Medicine 2011; 17(11):1381-90.

2.       McDonald B, Urrutia R, Yipp BG, Jenne CN, Kubes P. Intravascular neutrophil extracellular traps capture bacteria from the bloodstream during sepsis. Cell Host & Microbe 2012; 12(3):324-33.