Premium
Differential expression of IL‐10 receptor by epithelial cells and alveolar macrophages
Author(s) -
Lim S.,
Caramori G.,
Tomita K.,
Jazrawi E.,
Oates T.,
Chung K. F.,
Barnes P. J.,
Adcock I. M.
Publication year - 2004
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.2004.00455.x
Subject(s) - bronchoalveolar lavage , cytokine , immunology , interleukin , blot , stat1 , stat3 , receptor , interleukin 10 , biology , medicine , signal transduction , lung , interferon , microbiology and biotechnology , gene , biochemistry
Background: Interleukin (IL)‐10 is a pleiotropic cytokine with a broad spectrum of immunosuppressive and anti‐inflammatory effects. IL‐10 secretion from alveolar macrophages is defective in patients with asthma and lower concentrations of IL‐10 are found in bronchoalveolar lavage (BAL) from asthmatic patients than in normal control subjects. Reduced IL‐10 may result in exaggerated and more prolonged inflammatory responses in asthmatic airways. IL‐10 acting through the IL‐10 receptor (IL‐10R) stimulates the transcription factors STAT1 and STAT3. Methods: We investigated IL‐10 and IL‐10R expression in normal and asthmatic bronchial epithelium and BAL macrophages using reverse transcription‐polymerase chain reaction, immunohistochemistry and Western blotting. The functional effect of IL‐10 was examined using granulocyte–macrophage‐colony stimulating factor, enzyme‐linked immunosorbent assay and Western blotting for phosphorylated STAT1 and STAT3. Results: IL‐10 was not expressed in epithelial cells; furthermore these cells did not express the IL‐10R and had no functional response to exogenous IL‐10. Bronchial epithelial cells expressed variable levels of phosphorylated STAT1 and STAT3 with no change in expression between normal subjects and asthmatics. IL‐10 protein and IL‐10R expression was detected in alveolar macrophages from all subjects. Conclusion: Our study suggests that the bronchial epithelium is not a source of IL‐10 and cannot respond to exogenous IL‐10 because of a lack of IL‐10R expression.