Leukocyte recruitment after local endobronchial allergen challenge in asthma. Relationship to procedure and to airway interleukin-8 release.

We have investigated the profile of cellular recruitment into asthmatic airways after allergen and saline exposure and its relationship to interleukin-8 (IL-8) release. Fiberoptic bronchoscopy was used to instill allergen into the middle lobe while the right upper lobe received a sham saline challenge. Bronchoalveolar lavage (BAL) of both sites was performed either 4 or 24 h later. Neutrophil numbers in BAL fluid obtained 4 and 24 h after challenge were 17 and 48 times higher than prechallenge numbers (p < or = 0.001), but there was no statistically significant difference between the numbers of neutrophils at the two sites. In contrast, eosinophil numbers were increased by 6- and 20-fold, respectively, at 4 and 24 h at allergen-challenged as compared with saline-challenged sites (p < 0.005 and p < 0.02, respectively). Baseline concentrations of IL-8 in BAL fluid were undetectable in most cases. Four hours after allergen or saline exposure, BAL fluid IL-8 concentrations were: median, 200 pg/ml; range, 20 to 750 pg/ml and median, 123 pg/ml; range, < 20 to 800 pg/ml, respectively. These declined to 23 pg/ml (range, < 20 to 126 pg/ml) and 43 pg/ml (range < 20 to 130 pg/ml), respectively, 24 h after exposure. There was a significant correlation between neutrophil numbers and IL-8 concentrations 4 h after saline exposure. These findings indicate that neutrophil infiltration is a nonspecific response to the procedure of bronchoscopy and lavage, in contrast to eosinophil recruitment, which is an allergen-specific phenomenon, and it suggests that IL-8 release may be involved in neutrophil recruitment.

[1]  P. Howarth,et al.  Bronchial biopsy evidence for leukocyte infiltration and upregulation of leukocyte-endothelial cell adhesion molecules 6 hours after local allergen challenge of sensitized asthmatic airways. , 1994, The Journal of clinical investigation.

[2]  A. Wardlaw,et al.  Interleukin‐8 is a chemo‐attractant for eosinophils purified from subjects with a blood eosinophilia but not from normal healthy subjects , 1993, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[3]  P. Howarth,et al.  Immunolocalization of cytokines in the nasal mucosa of normal and perennial rhinitic subjects. The mast cell as a source of IL-4, IL-5, and IL-6 in human allergic mucosal inflammation. , 1993, Journal of immunology.

[4]  D. Schadendorf,et al.  Human mast cells produce IL-8. , 1993, Journal of immunology.

[5]  P. Howarth,et al.  Immunohistochemistry on resin sections: a comparison of resin embedding techniques for small mucosal biopsies. , 1993, Biotechnic & histochemistry : official publication of the Biological Stain Commission.

[6]  W. Busse,et al.  Increased airway inflammation with segmental versus aerosol antigen challenge. , 1993, The American review of respiratory disease.

[7]  R. Braun,et al.  Human peripheral blood eosinophils produce and release interleukin‐8 on stimulation with calcium ionophore , 1993, European journal of immunology.

[8]  A. Rot Neutrophil attractant/activation protein‐1 (interleukin‐8) induces in vitro neutrophil migration by haptotactic mechanism , 1993, European journal of immunology.

[9]  A. Kay,et al.  Expression and generation of interleukin-8, IL-6 and granulocyte-macrophage colony-stimulating factor by bronchial epithelial cells and enhancement by IL-1 beta and tumour necrosis factor-alpha. , 1992, Immunology.

[10]  T. Standiford,et al.  Pulmonary fibroblast expression of interleukin-8: a model for alveolar macrophage-derived cytokine networking. , 1991, American journal of respiratory cell and molecular biology.

[11]  R. Crystal,et al.  Interleukin-8 gene expression in human bronchial epithelial cells. , 1991, The Journal of biological chemistry.

[12]  E. Bleecker,et al.  Immediate and late inflammatory responses to ragweed antigen challenge of the peripheral airways in allergic asthmatics. Cellular, mediator, and permeability changes. , 1991, The American review of respiratory disease.

[13]  L. Koenderman,et al.  Modulation and induction of eosinophil chemotaxis by granulocyte- macrophage colony-stimulating factor and interleukin-3 , 1991 .

[14]  M. Baggiolini,et al.  Neutrophil Accumulation and Plasma Leakage Induced In Vivo by Neutrophil‐Activating Peptide‐1 , 1990, Journal of leukocyte biology.

[15]  W. Calhoun,et al.  Bronchoalveolar lavage in stable asthmatics does not cause pulmonary inflammation. , 1990, The American review of respiratory disease.

[16]  E. Leonard,et al.  Secretion of neutrophil attractant/activation protein by lipopolysaccharide-stimulated lung macrophages determined by both enzyme-linked immunosorbent assay and N-terminal sequence analysis. , 1990, The American review of respiratory disease.

[17]  J. Schröder,et al.  Secretion of novel and homologous neutrophil-activating peptides by LPS-stimulated human endothelial cells. , 1989, Journal of immunology.

[18]  A. Kay,et al.  The relationship between infiltrating CD4+ lymphocytes, activated eosinophils, and the magnitude of the allergen-induced late phase cutaneous reaction in man. , 1988, Journal of immunology.

[19]  R. Naclerio,et al.  Basophil influx occurs after nasal antigen challenge: effects of topical corticosteroid pretreatment. , 1988, The Journal of allergy and clinical immunology.

[20]  P. Moseley,et al.  Local allergen challenge and bronchoalveolar lavage of allergic asthmatic lungs. Description of the model and local airway inflammation. , 1987, The American review of respiratory disease.

[21]  S. Spector,et al.  Standardization of bronchial inhalation challenge procedures. , 1975, The Journal of allergy and clinical immunology.

[22]  M. Krangel,et al.  Biology and biochemistry of the chemokines: a family of chemotactic and inflammatory cytokines. , 1992, Critical reviews in immunology.