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
Comment
. 2020 Sep 7;217(9):e20201342.
doi: 10.1084/jem.20201342.

Blocking inflammation on the way: Rationale for CXCR2 antagonists for the treatment of COVID-19

Lars M Koenig  1 , Daniel F R Boehmer  1 , Philipp Metzger  1 , Max Schnurr  1 , Stefan Endres  1 , Simon Rothenfusser  1
Affiliations
Comment

Blocking inflammation on the way: Rationale for CXCR2 antagonists for the treatment of COVID-19

Lars M Koenig et al. J Exp Med. .

Abstract

An exacerbated and unbalanced immune response may account for the severity of COVID-19, the disease caused by the novel severe acute respiratory syndrome (SARS) coronavirus 2, SARS-CoV-2. In this Viewpoint, we summarize recent evidence for the role of neutrophils in the pathogenesis of COVID-19 and propose CXCR2 inhibition as a promising treatment option to block neutrophil recruitment and activation.

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
Infiltration and activation of neutrophils into SARS-CoV-2–infected lungs. Infected lung epithelial cells and inflammatory innate immune cells such as macrophages release the leukocyte attracting chemokines CXCL1, CXCL2, CXCL5, and CXCL8. Neutrophils are recruited and activated by these chemokines via their receptors CXCR1 and CXCR2. Subsequent release of antimicrobial effectors, such as ROS, proteases, and NETs, causes severe collateral damage in the lung. CXCR2 antagonists may inhibit lung damage by blockade of neutrophil migration and activation. Created with BioRender.
See this image and copyright information in PMC

Comment on

  • Immunology of COVID-19: Current State of the Science.
    Vabret N, Britton GJ, Gruber C, Hegde S, Kim J, Kuksin M, Levantovsky R, Malle L, Moreira A, Park MD, Pia L, Risson E, Saffern M, Salomé B, Esai Selvan M, Spindler MP, Tan J, van der Heide V, Gregory JK, Alexandropoulos K, Bhardwaj N, Brown BD, Greenbaum B, Gümüş ZH, Homann D, Horowitz A, Kamphorst AO, Curotto de Lafaille MA, Mehandru S, Merad M, Samstein RM; Sinai Immunology Review Project. Vabret N, et al. Immunity. 2020 Jun 16;52(6):910-941. doi: 10.1016/j.immuni.2020.05.002. Epub 2020 May 6. Immunity. 2020. PMID: 32505227 Free PMC article. Review.

References

    1. Barnes B.J., et al. . 2020. J. Exp. Med. 10.1084/jem.20200652 - DOI - PubMed
    1. Bikdeli B., et al. . 2020. J. Am. Coll. Cardiol. 10.1016/j.jacc.2020.04.031 - DOI - PubMed
    1. Blanco-Melo D., et al. . 2020. Cell. 10.1016/j.cell.2020.04.026 - DOI - PubMed
    1. Hastrup N., et al. . 2015. Cytokine. 10.1016/j.cyto.2015.01.002 - DOI - PubMed
    1. Horby P., et al. . 2020. medRxiv 10.1101/2020.06.22.20137273 (Preprint posted June 22, 2020) - DOI