Abstract:
:The mechanism by which IL-1 beta 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-1 beta. Having hypothesized that perivascular nitric oxide (NO) might modulate the effects of systemic IL-1 beta in the brain, we studied the expression of the genes encoding for IL-1 beta, 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-1 beta gene expression in the vascular wall, accompanied by perivascular induction of iNOS mRNA. We conclude that during systemic inflammation vascular IL-1 beta, 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-1 beta in the brain. We propose that the vascular and peri-vascular induction of iNOS mRNA by IL-1 beta might represent a mechanism for the modulation of the central nervous system effects of peripheral inflammatory mediators.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Wong ML,Bongiorno PB,al-Shekhlee A,Esposito A,Khatri P,Licinio Jdoi
10.1097/00001756-199611040-00008subject
Has Abstractpub_date
1996-11-04 00:00:00pages
2445-8issue
15-17eissn
0959-4965issn
1473-558Xjournal_volume
7pub_type
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