Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 May 12:8:550.
doi: 10.3389/fimmu.2017.00550. eCollection 2017.

A Role for Neutrophils in Viral Respiratory Disease

Jeremy V Camp  1 , Colleen B Jonsson  2
Affiliations
Review

A Role for Neutrophils in Viral Respiratory Disease

Jeremy V Camp et al. Front Immunol. .

Abstract

Neutrophils are immune cells that are well known to be present during many types of lung diseases associated with acute respiratory distress syndrome (ARDS) and may contribute to acute lung injury. Neutrophils are poorly studied with respect to viral infection, and specifically to respiratory viral disease. Influenza A virus (IAV) infection is the cause of a respiratory disease that poses a significant global public health concern. Influenza disease presents as a relatively mild and self-limiting although highly pathogenic forms exist. Neutrophils increase in the respiratory tract during infection with mild seasonal IAV, moderate and severe epidemic IAV infection, and emerging highly pathogenic avian influenza (HPAI). During severe influenza pneumonia and HPAI infection, the number of neutrophils in the lower respiratory tract is correlated with disease severity. Thus, comparative analyses of the relationship between IAV infection and neutrophils provide insights into the relative contribution of host and viral factors that contribute to disease severity. Herein, we review the contribution of neutrophils to IAV disease pathogenesis and to other respiratory virus infections.

Keywords: acute respiratory distress syndrome; influenza; neutrophil; respiratory virus; viral microenvironment.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Influenza A virus (IAV) infection in the upper respiratory tract. Infection of epithelial cells in the bronchus results in the release of type I interferons (IFN α/β) which signal to nearby cells. The result of IFN α/β signaling is the release of pro-inflammatory cytokines (e.g., IL-1β, IL-6, TNFα) that signal to endothelial cells, which help spread inflammatory signals (chemokines, such as CCL2, CCL5, CXCL8, CXCL10) throughout the blood to recruit innate immune cells to the site of infection. Recruited innate immune cells [such as natural killer cells (NK); monocytes (Mo); and neutrophils (NΦ)] must interact with activated endothelium to leave the blood stream and migrate toward the site of infection. There they can perform effector functions to control infection, such as releasing reactive oxygen species (ROS) and directly killing infected cells (cytolysis).
Figure 2
Figure 2
The course of disease following influenza A virus (IAV) infection. A timeline depicting major events in the viral replication cycle (red), the host immune response (blue), and the effects on the host tissue environment (green) during an IAV infection of the airways. A star marks the critical point for the formation of severe disease versus recovery from infection. This review posits that at this timepoint, coincident with a second wave of increasing neutrophilia and inflammation, the outcome of disease is determined.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Cowland JB, Borregaard N. Granulopoiesis and granules of human neutrophils. Immunol Rev (2016) 273:11–28.10.1111/imr.12440 - DOI - PubMed
    1. Galani IE, Andreakos E. Neutrophils in viral infections: current concepts and caveats. J Leukoc Biol (2015) 98:557–64.10.1189/jlb.4VMR1114-555R - DOI - PubMed
    1. Abraham E. Neutrophils and acute lung injury. Crit Care Med (2003) 31:S195–9.10.1097/01.CCM.0000057843.47705.E8 - DOI - PubMed
    1. Burns AR, Smith CW, Walker DC. Unique structural features that influence neutrophil emigration into the lung. Physiol Rev (2003) 83:309–36.10.1152/physrev.00023.2002 - DOI - PubMed
    1. Grommes J, Soehnlein O. Contribution of neutrophils to acute lung injury. Mol Med (2011) 17:293–307.10.2119/molmed.2010.00138 - DOI - PMC - PubMed

LinkOut - more resources