1. Metabolic regulation by prostaglandin E
- Author
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Calum T, Robb, You, Zhou, Jennifer M, Felton, Birong, Zhang, Marie, Goepp, Privjyot, Jheeta, Danielle J, Smyth, Rodger, Duffin, Sonja, Vermeren, Richard M, Breyer, Shuh, Narumiya, Henry J, McSorley, Rick M, Maizels, Jürgen K J, Schwarze, Adriano G, Rossi, and Chengcan, Yao
- Abstract
Group 2 innate lymphoid cells (ILC2s) play a critical role in asthma pathogenesis. Non-steroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (NERD) is associated with reduced signaling via EP2, a receptor for prostaglandin EThe roles of PGEDeficiency of EP2 rather than EP4 augments IL-33-induced mouse lung ILC2 responses and eosinophilic inflammation in vivo. In contrast, exogenous agonism of EP4 and EP2 or inhibition of phosphodiesterase markedly restricts IL-33-induced lung ILC2 responses. Mechanistically, PGEWe have defined a mechanism for optimal suppression of mouse lung ILC2 responses by endogenous PGE
- Published
- 2022