Abstract
The mechanism by which IL-1β exerts its actions in the brain during systemic inflammation is not fully understood, as neither IL-1 receptor gene expression nor IL-1 binding have been identified in significant levels in key areas that respond to IL-1β. Having hypothesized that perivascular nitric oxide (NO) might modulate the effects of systemic IL-1β in the brain, we studied the expression of the genes encoding for IL-1β, the signal-transducing IL-1 receptor type I (IL-1RI) and inducible NO synthase (iNOS) constitutively and during systemic inflammation in vascular and perivascular regions of the rat brain. Our results show that IL-1RI is constitutively expressed at the interface of the vascular wall and perivascular glia. During systemic inflammation there is induction of IL-1β gene expression in the vascular wall, accompanied by perivascular induction of iNOS mRNA. We conclude that during systemic inflammation vascular IL-1β, binding to vascular and perivascular IL-1RI receptors, may induce perivascular iNOS gene expression, leading to the production of NO and modulation of the effects of IL-1β in the brain. We propose that the vascular and perivascular induction of iNOS mRNA by IL-1β might represent a mechanism for the modulation of the central nervous system effects of peripheral inflammatory mediators.
Original language | English |
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Pages (from-to) | 2445-2448 |
Number of pages | 4 |
Journal | NeuroReport |
Volume | 7 |
Issue number | 15-17 |
DOIs | |
Publication status | Published or Issued - 1996 |
Externally published | Yes |
Keywords
- Brain vasculature
- In situ hybridization Interleukin-1
- Interleukin-1 receptors
- Lipopolysaccharide
- Nitric oxide
- Nitric oxide synthase
- Sepsis
ASJC Scopus subject areas
- General Neuroscience