Interleukin-6 and interleukin-1α production is associated with antigen-induced late nasal response

https://doi.org/10.1016/0091-6749(93)90066-OGet rights and content

Abstract

Background: Cytokines such as tumor necrosis factor (TNF)-α interleukin (IL)-1α IL-6 and granulocyte macrophage-colony stimulating factor (GM-CSF) are able to potentiate allergic inflammation and seem to be implicated in the development of the late allergic reaction.

Methods: To study the time course of cytokine production, sequential lavages were performed after nasal allergen challenge. Thirteen patients with allergic rhinitis and four healthy subjects were exposed to grass pollen (n = 6 and n = 2, respectively) or dust mite allergen (n = 7 and n = 2, respectively).

Results: Among the patients with allergic rhinitis, a single early response (single responders) developed in four, eight exhibited a dual response (dual responders) and one patient as well as the four healthy subjects did not respond. In addition to the measurement of IL-1 α, IL-6, TNF-α and GM-CSF concentrations by ELISA, the release of histamine, tryptase, and cosinophil cationic protein was also evaluated by radioimmunoassay performed on nasal lavage fluids. Concerning meditor levels in nasal lavage fluid, neither histamine release nor cytokine elevation were noted in healthy subjects. As previously described, histamine, tryptase and eosinophil cationic protein were released in single and dual responders. Concerning cytokines, TNF-α was undetectable in the majority of nasal lavages and an increase in GM-CSF concentration was occasionally observed whatever the type of response. In contrast, an increase in IL-1α and IL-6 levels was observed for dual responders during the early period (12.6 ± 3 and 9.2 ± 2 pg/ml, respectively; p < 0.01 (in both cases) and at a higher level during the late period (14.5 ± 4, p not significant and 16.7 ± 8 pglml, respectively; p < 0.01) when compared with baseline values (72 ± 2.2 and 2 ± 0.7 pg/ml respectively). For single responders IL-1α and IL-6 secretion was detected mainly during the early period.

Conclusion: These data suggest a role for IL-1 a in the induction and perennisation of the inflammatory reaction in allergic rhinitis; whereas the role of IL-6 remains to be investigated.

References (38)

  • R.M. Naclerio et al.

    Inflammatory mediators in late antigen-induced rhinitis

    N Engl J Med

    (1985)
  • M.R. Shaafsma et al.

    Interleukin-1 synergizes with granulocyte-macrophage colony-stimulating factor on granulocytic colony formation by intermediate production of granulocyte colony-stimulating factor

    Blood

    (1989)
  • A.M. Lamas et al.

    Studies on the adhesive interaction between purified eosinophils and cultured vascular endothelial cells

    J Immunol

    (1988)
  • J.S. Pober et al.

    Overlapping patterns of activation of human endothelial cells by interleukin 1, tumor necrosis factor, and immune interferon

    J Immunol

    (1986)
  • R.J. Debs et al.

    Lung-specific delivery of cytokines induces sustained pulmonary and systemic immuno-modulation in rats

    J Immunol

    (1989)
  • T.J. Sayers et al.

    Effect of cytokines on polymorphonuclear neutrophil infiltration in the mouse

    J Immunol

    (1988)
  • D.S. Silberstein et al.

    TNF enhances eosinophil toxicity to Schistosoma mansoni larvae

  • S.H. Pincus et al.

    Interaction of IL 1 and TPA in modulation of eosinophil function

    J Immunol

    (1986)
  • S.J. Klebanoff et al.

    Stimulation of neutrophils by tumor necrosis factor

    J Immunol

    (1986)
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