| First Author | Matsuwaki T | Year | 2017 |
| Journal | Brain Behav Immun | Volume | 66 |
| Pages | 165-176 | PubMed ID | 28655587 |
| Mgi Jnum | J:253472 | Mgi Id | MGI:6109683 |
| Doi | 10.1016/j.bbi.2017.06.013 | Citation | Matsuwaki T, et al. (2017) Involvement of interleukin-1 type 1 receptors in lipopolysaccharide-induced sickness responses. Brain Behav Immun 66:165-176 |
| abstractText | Sickness responses to lipopolysaccharide (LPS) were examined in mice with deletion of the interleukin (IL)-1 type 1 receptor (IL-1R1). IL-1R1 knockout (KO) mice displayed intact anorexia and HPA-axis activation to intraperitoneally injected LPS (anorexia: 10 or 120microg/kg; HPA-axis: 120microg/kg), but showed attenuated but not extinguished fever (120microg/kg). Brain PGE2 synthesis was attenuated, but Cox-2 induction remained intact. Neither the tumor necrosis factor-alpha (TNFalpha) inhibitor etanercept nor the IL-6 receptor antibody tocilizumab abolished the LPS induced fever in IL-1R1 KO mice. Deletion of IL-1R1 specifically in brain endothelial cells attenuated the LPS induced fever, but only during the late, 3rd phase of fever, whereas deletion of IL-1R1 on neural cells or on peripheral nerves had little or no effect on the febrile response. We conclude that while IL-1 signaling is not critical for LPS induced anorexia or stress hormone release, IL-1R1, expressed on brain endothelial cells, contributes to the febrile response to LPS. However, also in the absence of IL-1R1, LPS evokes a febrile response, although this is attenuated. This remaining fever seems not to be mediated by IL-6 receptors or TNFalpha, but by some yet unidentified pyrogenic factor. |
