Interaction between interleukin 1beta and endogenous neurokinin 1 receptor agonists in mediating plasma extravasation and neutrophil accumulation in the cutaneous microvasculature of the rat

Interleukin 1beta (IL-1beta) is a potent mediator of neutrophil accumulation. Antidromic stimulation of the rat saphenous nerve leads to neurogenic oedema formation mediated by endogenous tachykinins. Here, we have investigated links between IL-1beta and the tachykinin 1 (NK(1)) receptors in microva...

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Bibliographic Details
Published in:	Neuroscience letters Vol. 318; no. 1; pp. 13 - 16
Main Authors:	Pintér, Erika, Thán, Márta, Chu, D Quyen, Fogg, Caraline, Brain, Susan D
Format:	Journal Article
Language:	English
Published:	Ireland 18-01-2002
Subjects:	Animals Edema - metabolism Electric Stimulation Interleukin-1 - pharmacology Male Microcirculation - physiology Neuritis - metabolism Neurokinin-1 Receptor Antagonists Neutrophils - cytology Neutrophils - drug effects Piperidines - pharmacology Plasma - metabolism Quinuclidines - pharmacology Rats Rats, Wistar Receptors, Neurokinin-1 - agonists Receptors, Neurokinin-1 - metabolism Sciatic Nerve - physiology Sensory Receptor Cells - physiology Skin - blood supply Skin - immunology Skin - innervation Tachykinins - metabolism
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Summary:	Interleukin 1beta (IL-1beta) is a potent mediator of neutrophil accumulation. Antidromic stimulation of the rat saphenous nerve leads to neurogenic oedema formation mediated by endogenous tachykinins. Here, we have investigated links between IL-1beta and the tachykinin 1 (NK(1)) receptors in microvascular events in rat skin. Saphenous nerve-induced plasma extravasation was not modulated by skin pretreatment with IL-1beta (3 pmol/site intradermally). In addition, the long-lasting antidromic electrical stimulation did not induce significant neutrophil accumulation in naive rat skin. By comparison, the effect of IL-1beta-induced neutrophil accumulation was significantly potentiated by co-stimulation of the ipsilateral saphenous nerve; an effect prevented by an NK(1) receptor antagonist (SR140333, 480 nmol/kg, i.v.). We conclude that IL-1beta-induced neutrophil accumulation can be influenced in a pro-inflammatory manner by ongoing neurogenic inflammation, of relevance to the sensory nerve input that occurs during ongoing inflammatory disease.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0304-3940