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ILC3 pyroptosis limits Salmonella infection

Nature Microbiology volume 7, pages 933–934 (2022)Cite this article

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Enteric Salmonella not only activates the ILC3–IL-22 axis upon infection to provide a competitive advantage over resident microbiota but also invades ILC3s and induces inflammatory cell death, thus limiting infection.

Group 3 innate lymphoid cells (ILC3s) are the primary source of interleukin-22 (IL-22), an essential cytokine for innate antimicrobial responses in the gut. Salmonella can exploit the IL-22 pathway to enhance infection. Writing in Nature Microbiology1, Xiong et al. report that Salmonella infects ILC3s at later stages of the infection, which induces pyroptosis and controls bacterial infection.

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Fig. 1: Biphasic response of ILC3s to enteric Salmonella infection.

References

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Authors and Affiliations

  1. Joan and Sanford I. Weill Department of Medicine, Division of Gastroenterology and Hepatology, Weill Cornell Medicine, Cornell University, New York, NY, USA

    Ann M. Joseph & Gregory F. Sonnenberg

  2. Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY, USA

    Ann M. Joseph & Gregory F. Sonnenberg

  3. Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA

    Ann M. Joseph & Gregory F. Sonnenberg

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  1. Ann M. Joseph
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  2. Gregory F. Sonnenberg
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Correspondence to Gregory F. Sonnenberg.

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The authors declare no competing interests.

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Joseph, A.M., Sonnenberg, G.F. ILC3 pyroptosis limits Salmonella infection. Nat Microbiol 7, 933–934 (2022). https://doi.org/10.1038/s41564-022-01165-1

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