Impaired febrile response in mice lacking the prostaglandin E receptor subtype EP3

Fumitaka Ushikubi, Eri Segi, Yukihiko Sugimoto, Takahiko Murata, Toshiyuki Matsuoka, Takuya Kobayashi, Hiroko Hizaki, Kazuhito Tuboi, Masato Katsuyama, Atsushi Ichikawa, Takashi Tanaka, Nobuaki Yoshida and Shuh Narumiya ()
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Fumitaka Ushikubi: Faculty of Medicine, Faculty of Pharmaceutical Sciences, Kyoto University
Eri Segi: Faculty of Pharmaceutical Sciences, Kyoto University
Yukihiko Sugimoto: Faculty of Pharmaceutical Sciences, Kyoto University
Takahiko Murata: Faculty of Medicine, Faculty of Pharmaceutical Sciences, Kyoto University
Toshiyuki Matsuoka: Faculty of Medicine, Faculty of Pharmaceutical Sciences, Kyoto University
Takuya Kobayashi: Faculty of Medicine, Faculty of Pharmaceutical Sciences, Kyoto University
Hiroko Hizaki: Faculty of Pharmaceutical Sciences, Kyoto University
Kazuhito Tuboi: Faculty of Pharmaceutical Sciences, Kyoto University
Masato Katsuyama: Faculty of Pharmaceutical Sciences, Kyoto University
Atsushi Ichikawa: Faculty of Pharmaceutical Sciences, Kyoto University
Takashi Tanaka: Research Institute, Osaka Medical Center for Maternal and Child Health
Nobuaki Yoshida: Research Institute, Osaka Medical Center for Maternal and Child Health
Shuh Narumiya: Faculty of Medicine, Faculty of Pharmaceutical Sciences, Kyoto University

Nature, 1998, vol. 395, issue 6699, 281-284

Abstract: Abstract Fever, a hallmark of disease, is elicited by exogenous pyrogens, that is, cellular components, such as lipopolysaccharide (LPS), of infectious organisms, as well as by non-infectious inflammatory insults. Both stimulate the production of cytokines, such as interleukin (IL)-1β, that act on the brain as endogenous pyrogens1. Fever can be suppressed by aspirin-like anti-inflammatory drugs. As these drugs share the ability to inhibit prostaglandin biosynthesis2, it is thought that a prostaglandin is important in fever generation. Prostaglandin E2 (PGE2) may be a neural mediator of fever3, but this has been much debated1,4,5,6,7. PGE2 acts by interacting with four subtypes of PGE receptor, the EP1, EP2, EP3 and EP4 receptors8. Here we generate mice lacking each of these receptors by homologous recombination. Only mice lacking the EP3 receptor fail to show a febrile response to PGE2 and to either IL-1β or LPS. Our results establish that PGE2 mediates fever generation in response to both exogenous and endogenous pyrogens by acting at the EP3 receptor.

Date: 1998
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DOI: 10.1038/26233

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