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American Association for the Advancement of Science, Science, 6279(351), p. 1333-1338, 2016

DOI: 10.1126/science.aad9903

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Prostaglandin E <sub>2</sub> constrains systemic inflammation through an innate lymphoid cell–IL-22 axis

Journal article published in 2016 by Rodger Duffin, Richard A. O’Connor, Siobhan Crittenden, Thorsten Forster, Cunjing Yu, Xiaozhong Zheng, Danielle Smyth ORCID, Calum T. Robb, Fiona Rossi, Christos Skouras, Shaohui Tang, James Richards, Antonella Pellicoro, Richard B. Weller, Richard M. Breyer and other authors.
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Abstract

A prostaglandin barrier to inflammation Blood-borne bacterial infections and severe trauma can send the immune system into overdrive, causing it to pump out inflammatory mediators, sometimes at lethal doses. Duffin et al. now report on a role for prostaglandins in keeping systemic inflammation in check. Systemic inflammation correlates with decreased production of the prostaglandin E2 (PGE2). Blocking PGE2 signaling in mice led to severe inflammation associated with the translocation of gut bacteria. PGE2 acts on innate lymphoid cells, which produce interleukin-22, a secreted protein that helps promote intestinal integrity. Science , this issue p. 1333