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

Erika Pintér, Márta Thán, D. Quyen Chu, Caraline Fogg, Susan D. Brain

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11 Citations (Scopus)


Interleukin 1 β (IL-1 β) 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-1 β and the tachykinin 1 (NK1) receptors in microvascular events in rat skin. Saphenous nerve-induced plasma extravasation was not modulated by skin pretreatment with IL-1 β (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-1 β-induced neutrophil accumulation was significantly potentiated by co-stimulation of the ipsilateral saphenous nerve; an effect prevented by an NK1 receptor antagonist (SR140333, 480 nmol/kg, i.v.). We conclude that IL-1 β-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.

Original languageEnglish
Pages (from-to)13-16
Number of pages4
JournalNeuroscience Letters
Issue number1
Publication statusPublished - Jan 18 2002



  • Antidromic nerve stimulation
  • Interleukin 1 β
  • Neurogenic inflammation
  • Neurokinin 1 receptor
  • Neutrophil accumulation
  • Plasma extravasation

ASJC Scopus subject areas

  • Neuroscience(all)

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