Basophil recruitment and IL-4 production during human allergen-induced late asthma

J Allergy Clin Immunol. 2001 Aug;108(2):205-11. doi: 10.1067/mai.2001.117175.

Abstract

Background: Basophils represent an important source of inflammatory mediators and cytokines after IgE-dependent activation in human beings.

Objective: To assess the role of basophils in allergic asthma, we measured the number of basophils in the bronchial mucosa and their capacity to express IL-4 mRNA and protein during allergen-induced late asthmatic responses.

Methods: Fiberoptic bronchoscopic bronchial biopsies were obtained at 24 hours from sites of segmental bronchial allergen challenge and control sites in 19 patients with atopic asthma and 6 nonatopic healthy volunteers. Basophil numbers were assessed by immunohistochemistry through use of mAb 2D7. IL-4 mRNA--positive cells were detected through use of in situ hybridization and colocalized to basophils through use of sequential immunohistochemistry/in situ hybridization. IL-4 protein was detected and colocalized to basophils through use of dual immunohistochemistry.

Results: After allergen challenge, there was an increase in the median number of 2D7-positive basophils per square millimeter in the bronchial mucosa in patients with asthma (0.9 cells/mm(2) at baseline to 8.8 cells/mm(2) after challenge; P =.002), which also was significantly higher than what was seen in nonasthmatic controls (P =.01). Similarly, IL-4 mRNA--positive cells were increased at 24 hours in patients with asthma (1.4 to 14) in comparison with controls (0 to 0; P =.02). Colocalization studies revealed that 15% and 41% of the basophil population in patients with asthma after allergen-challenge expressed, respectively, IL-4 mRNA and protein. Conversely, 19% of IL-4 mRNA-positive cells and 72% of IL-4 protein--positive cells were accounted for by basophils.

Conclusion: After allergen provocation in sensitive patients with atopic asthma, basophils are recruited to the bronchial mucosa and express IL-4 mRNA and protein, which might contribute to local IgE synthesis and/or tissue eosinophilia or other aspects of allergic inflammation during late responses and ongoing asthma.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Asthma / immunology*
  • Basophils / immunology*
  • Bronchi / immunology
  • Chemotaxis, Leukocyte
  • Female
  • Humans
  • Hypersensitivity, Immediate / immunology
  • Immunohistochemistry
  • In Situ Hybridization
  • Interleukin-4 / biosynthesis*
  • Interleukin-4 / genetics
  • Male
  • RNA, Messenger / isolation & purification
  • Respiratory Mucosa / immunology

Substances

  • RNA, Messenger
  • Interleukin-4