Potential role of interleukin-1 in allergen-induced late asthmatic reactions in guinea pigs: suppressive effect of interleukin-1 receptor antagonist on late asthmatic reaction

J Allergy Clin Immunol. 1995 Jun;95(6):1236-45. doi: 10.1016/s0091-6749(95)70081-1.


Interleukin (IL)-1 is a pluripotential proinflammatory cytokine and is thought to be involved in the pathogenesis of bronchial asthma and late asthmatic reactions (LARs). To determine whether IL-1 plays a role in LAR, guinea pigs sensitized with Ascaris antigen were used. We evaluated IL-1 production by immunostaining with anti-IL-1 beta antibody and elucidated the action of IL-1 in LAR with recombinant IL-1 receptor antagonist. Immunostaining revealed that IL-1 beta-like immunoreactivity-positive cells increased in the airway walls and in bronchoalveolar lavage fluid after the antigen challenge. IL-1 receptor antagonist protein pretreatment reduced the generation of LAR in terms of pulmonary resistance. IL-1 receptor antagonist protein pretreatment did not change cellular components but reduced the percentage of hypodense eosinophils in bronchoalveolar lavage fluid. We also studied the direct effect of recombinant human IL-1 beta on pulmonary resistance and eosinophil activity measured as released eosinophil peroxidase activity. Recombinant human IL-1 beta did not change pulmonary resistance but primed eosinophils to release eosinophil peroxidase activity in response to platelet activating factor. Therefore these results suggest that IL-1 was produced in sensitized pulmonary tissue of guinea pigs by allergen exposure and played a role in the generation of LAR, at least partially by modulating the activation of eosinophils.

MeSH terms

  • Animals
  • Asthma / immunology*
  • Asthma / metabolism
  • Asthma / physiopathology
  • Bronchoalveolar Lavage Fluid / immunology*
  • Cell Count
  • Eosinophils / drug effects
  • Eosinophils / pathology
  • Guinea Pigs
  • Humans
  • Immunohistochemistry
  • Interleukin-1 / analysis*
  • Receptors, Interleukin-1 / antagonists & inhibitors*
  • Recombinant Proteins / pharmacology
  • Trachea / metabolism
  • Trachea / pathology


  • Interleukin-1
  • Receptors, Interleukin-1
  • Recombinant Proteins