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Licence: Creative Commons: Attribution (CC-BY)
| Original language | English |
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| Journal | Thorax |
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| Early online date | 24 Mar 2018 |
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| DOIs | |
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| Publication status | E-pub ahead of print - 24 Mar 2018 |
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Acute lung injury (ALI) is neutrophil-dominant, life-threatening disease without effective therapies and better understanding of the pathophysiological mechanisms involved is an urgent need. Here we show that IL-22 is produced from innate lymphoid cells (ILCs) and is responsible for suppression of experimental lung neutrophilic inflammation. Blocking prostaglandin E2 (PGE2) synthesis reduces lung ILCs and IL-22 production, resulting in exacerbation of lung neutrophilic inflammation. In contrast, activation of the PGE2 receptor EP4 prevents acute lung inflammation. We thus demonstrate a mechanism for production of innate IL-22 in the lung during acute injury, highlighting potential therapeutic strategies for control of lung neutrophilic inflammation by targeting the PGE2/ILC/IL-22 axis.
ID: 54253473
