Skip to main content

Thank you for visiting 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.

Neonatal sepsis

The proinflammatory cytokine IL-18 is elevated in both normal neonates and those with sepsis, in whom it has a deleterious role. In the Proceedings of the National Academy of Sciences USA, Moore and colleagues use a neonatal mouse model of polymicrobial sepsis to investigate the mechanistic basis of IL-18's function in sepsis. IL-18-deficient mice are resistant to sepsis, and exogenous supply of this cytokine worsens the outcome of sepsis, increases the bacterial load in the peritoneum and manifests as damage to the gut ileum. Mechanistically, IL-18 activates secretion of the proinflammatory cytokine IL-17A by γδ T cells, and it is this that worsens symptoms in this model of sepsis. These data reveal an unexpected pathway involved in the pathology of neonatal sepsis and might lead to new drug targets in this otherwise nearly intractable condition.

Proc. Natl. Acad. Sci. USA (25 April 2016) doi:10.1073/pnas.1515793113


Rights and permissions

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Fehervari, Z. Neonatal sepsis. Nat Immunol 17, 617 (2016).

Download citation

  • Published:

  • Issue Date:

  • DOI:


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