The involvement of prostaglandin E2 in interleukin-1β evoked anorexia is strain dependent
2017 (English)In: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 60, 27-31 p.Article in journal (Refereed) Published
From experiments in mice in which the prostaglandin E2 (PGE2) synthesizing enzyme mPGES-1 was genetically deleted, as well as from experiments in which PGE2 was injected directly into the brain, PGE2 has been implicated as a mediator of inflammatory induced anorexia. Here we aimed at examining which PGE2 receptor (EP1–4) that was critical for the anorexic response to peripherally injected interleukin-1β (IL-1β). However, deletion of neither EP receptor in mice, either globally (for EP1, EP2, and EP3) or selectively in the nervous system (EP4), had any effect on the IL-1β induced anorexia. Because these mice were all on a C57BL/6 background, whereas previous observations demonstrating a role for induced PGE2 in IL-1β evoked anorexia had been carried out on mice on a DBA/1 background, we examined the anorexic response to IL-1β in mice with deletion of mPGES-1 on a C57BL/6 background and a DBA/1 background, respectively. We confirmed previous findings that mPGES-1 knock-out mice on a DBA/1 background displayed attenuated anorexia to IL-1β; however, mice on a C57BL/6 background showed the same profound anorexia as wild type mice when carrying deletion of mPGES-1, while displaying almost normal food intake after pretreatment with a cyclooxygenase-2 inhibitor. We conclude that the involvement of induced PGE2 in IL-1β evoked anorexia is strain dependent and we suggest that different routes that probably involve distinct prostanoids exist by which inflammatory stimuli may evoke an anorexic response and that these routes may be of different importance in different strains of mice.
Place, publisher, year, edition, pages
Academic Press, 2017. Vol. 60, 27-31 p.
Anorexia, Prostaglandin E2, EP receptors, Interleukin-1, Cyclooxygenase-2, Mice
Immunology Cell Biology Pharmacology and Toxicology
IdentifiersURN: urn:nbn:se:liu:diva-132639DOI: 10.1016/j.bbi.2016.06.014ISI: 000391908200004PubMedID: 27375005OAI: oai:DiVA.org:liu-132639DiVA: diva2:1047665
Funding agencies: Swedish Research Council [07879, 20725]; Swedish Cancer Foundation [213/692]; County Council of Ostergotland; Knut and Alice Wallenberg Foundation2016-11-182016-11-182017-03-13Bibliographically approved