| First Author | Wilhelms DB | Year | 2014 |
| Journal | J Neurosci | Volume | 34 |
| Issue | 35 | Pages | 11684-90 |
| PubMed ID | 25164664 | Mgi Jnum | J:216148 |
| Mgi Id | MGI:5607804 | Doi | 10.1523/JNEUROSCI.1838-14.2014 |
| Citation | Wilhelms DB, et al. (2014) Deletion of prostaglandin E2 synthesizing enzymes in brain endothelial cells attenuates inflammatory fever. J Neurosci 34(35):11684-90 |
| abstractText | Fever is a hallmark of inflammatory and infectious diseases. The febrile response is triggered by prostaglandin E2 synthesis mediated by induced expression of the enzymes cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase 1 (mPGES-1). The cellular source for pyrogenic PGE2 remains a subject of debate; several hypotheses have been forwarded, including immune cells in the periphery and in the brain, as well as the brain endothelium. Here we generated mice with selective deletion of COX-2 and mPGES1 in brain endothelial cells. These mice displayed strongly attenuated febrile responses to peripheral immune challenge. In contrast, inflammation-induced hypoactivity was unaffected, demonstrating the physiological selectivity of the response to the targeted gene deletions. These findings demonstrate that PGE2 synthesis in brain endothelial cells is critical for inflammation-induced fever. |
