Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Correspondence
  • Published:

Neutrophils are not required for resolution of acute gouty arthritis in mice

Nature Medicine volume 22, pages 1382–1384 (2016)Cite this article

Subjects

To the Editor:

Gout is triggered when the deposition of monosodium urate (MSU) crystals in joints induces acute inflammation characterized by the recruitment of neutrophils1,2. Attacks of gout resolve in days, despite the persistence of crystals in structures called tophi, but the mechanisms that underlie this rapid resolution of inflammation are unknown1,3. Recently, Schauer et al.4 reported that neutrophil extracellular traps (NETs, referred to by Schauer et al.4 as aggNETs) present in tophi can resolve inflammation in gout by degrading proinflammatory mediators.

This is a preview of subscription content, access via your institution

Relevant articles

Open Access articles citing this article.

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1: MSU crystals can form aggregates in mice markedly deficient in neutrophils.
Figure 2: The depletion of neutrophils with anti-Gr-1 antibodies diminishes MSU-crystal-induced paw edema in mice.

References

  1. Martin, W.J. & Harper, J.L. Immunol. Cell Biol. 88, 15–19 (2010).

    Article  Google Scholar 

  2. Mitroulis, I., Kambas, K. & Ritis, K. Semin. Immunopathol. 35, 501–512 (2013).

    Article  CAS  Google Scholar 

  3. Steiger, S. & Harper, J.L. Curr. Rheumatol. Rep. 16, 392 (2014).

    Article  Google Scholar 

  4. Schauer, C. et al. Nat. Med. 20, 511–517 (2014).

    Article  CAS  Google Scholar 

  5. Gross, S. et al. Nat. Med. 15, 455–461 (2009).

    Article  CAS  Google Scholar 

  6. Reber, L.L. et al. Arthritis Rheumatol. 66, 2881–2891 (2014).

    Article  CAS  Google Scholar 

Download references

Acknowledgements

L.L.R. acknowledges support from the Arthritis National Research Foundation (ANRF), the US National Institutes of Health (grant K99AI110645), the European Commission Marie Skłodowska-Curie Individual Fellowship (H2020-MSCA-IF-2014 656086) and the French 'Institut National de la Santé et de la Recherche Médicale' (INSERM); N.G. is the recipient of a fellowship from the French “Fondation pour la Recherche Médicale FRM” and the Philippe Foundation; P.S. is supported by a Max Kade Fellowship of the Max Kade Foundation and the Austrian Academy of Sciences and a Schroedinger Fellowship of the Austrian Science Fund (FWF) (J3399-B21); S.J.G. acknowledges support from the US National Institutes of Health (grants R01 AR067145, U19 AI104209, NS 080062), the Tobacco-Related Disease Research Program at the University of California and the Department of Pathology, Stanford University School of Medicine.

Author information

Author notes

  1. Philipp Starkl

    Present address: Current address: CeMM, Research Center for Molecular Medicine of the Austrian Academy of Sciences, and Department of Medicine I, Research Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria.,

Authors and Affiliations

  1. Department of Pathology, Stanford University School of Medicine, Stanford, California, USA

    Laurent L Reber, Nicolas Gaudenzio, Philipp Starkl & Stephen J Galli

  2. Département d'Immunologie, Unité des Anticorps en Thérapie et Pathologie, Institut Pasteur, Paris, France

    Laurent L Reber

  3. Institut National de la Santé et de la Recherche Médicale, Paris, U1222, France

    Laurent L Reber

  4. Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, California, USA

    Nicolas Gaudenzio & Stephen J Galli

  5. Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA

    Stephen J Galli

Authors
  1. Laurent L Reber
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Nicolas Gaudenzio
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Philipp Starkl
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Stephen J Galli
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

L.L.R. and S.J.G conceived the project. L.L.R., N.G., P.S. and S.J.G. were involved in experimental design. L.L.R. performed most of the experiments, analyzed and compiled the data. N.G. and P.S. helped with experiments. All authors participated in writing or editing the paper.

Corresponding authors

Correspondence to Laurent L Reber or Stephen J Galli.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

Supplementary information

Supplementary Figures

Supplementary Figures 1–6 (PDF 1979 kb)

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Reber, L., Gaudenzio, N., Starkl, P. et al. Neutrophils are not required for resolution of acute gouty arthritis in mice. Nat Med 22, 1382–1384 (2016). https://doi.org/10.1038/nm.4216

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nm.4216

This article is cited by

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing