Endothelial cells of the rat brain vasculature express cyclooxygenase-2 mRNA in response to systemic interleukin-1 beta: a possible site of prostaglandin synthesis responsible for fever

Brain Res. 1996 Sep 16;733(2):263-72. doi: 10.1016/0006-8993(96)00575-6.

Abstract

We previously showed that intraperitoneal injection of lipopolysaccharide induced cyclooxygenase-2 (COX-2) mRNA in as yet unidentified cells of blood vessels and leptomeninges in the rat brain and proposed a possible role of these cells as the source of prostaglandin E2 in the genesis of fever (Cao et al., Brain Res., 697 (1995) 187-196). In the present study, to proceed further with this line of research, we addressed the following two questions: first, does a pyrogenic dose of interleukin-1 beta (IL-1 beta), an endogenous pyrogen, induce COX-2 mRNA in the brain blood vessels and leptomeninges? Secondly, if it does, what type of cells are positive for COX-2 mRNA? Intraperitoneal injection of recombinant human IL-1 beta (30 micrograms/kg) induced fever in rats and an in situ hybridization study revealed that faint but significant COX-2 mRNA signals appeared in the blood vessels and leptomeninges at 1.5 h after the injection (the early rising phase of fever). The mRNA signals increased in number and intensity at 4 h (early plateau phase), decreased at 6.5 h (early recovery phase), and completely disappeared by 10 h after the injection (late recovery phase). The COX-2 mRNA positive cells in the blood vessels were likely to be the endothelial cells since the corresponding cells in the adjacent mirror-imaged section also expressed mRNAs for intracellular adhesion molecule-1 and the type-I interleukin-1 receptor, although those in the leptomeninges still remained unidentified. These results imply that circulating IL-1 beta acts on its receptor on the endothelial cells of the brain vasculature to induce COX-2 mRNA, which is possibly responsible for the elevated level of PGE2 seen during fever.

MeSH terms

  • Animals
  • Autoradiography
  • Body Temperature / drug effects
  • Cerebrovascular Circulation*
  • Cyclooxygenase 2
  • Dinoprostone / physiology
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / enzymology*
  • Endothelium, Vascular / immunology*
  • Fever / physiopathology*
  • Gene Expression Regulation / drug effects
  • Humans
  • In Situ Hybridization
  • Interleukin-1 / pharmacology*
  • Isoenzymes / biosynthesis*
  • Lipopolysaccharides / toxicity
  • Male
  • Membrane Proteins
  • Meninges / blood supply*
  • Prostaglandin-Endoperoxide Synthases / biosynthesis*
  • Prostaglandins / biosynthesis*
  • RNA, Messenger / biosynthesis
  • Rats
  • Rats, Wistar
  • Receptors, Interleukin-1 / biosynthesis
  • Recombinant Proteins / pharmacology
  • Sulfur Radioisotopes
  • Time Factors
  • Transcription, Genetic / drug effects*

Substances

  • Interleukin-1
  • Isoenzymes
  • Lipopolysaccharides
  • Membrane Proteins
  • Prostaglandins
  • RNA, Messenger
  • Receptors, Interleukin-1
  • Recombinant Proteins
  • Sulfur Radioisotopes
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases
  • Dinoprostone