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Induction of IL‐6 in co‐culture of bronchial epithelial cells and eosinophils is regulated by p38 MAPK and NF‐ κ B
Author(s) -
Wang C. B.,
Wong C. K.,
Ip W. K.,
Li M. L. Y.,
Tian Y. P.,
Lam C. W. K.
Publication year - 2005
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.1398-9995.2005.00884.x
Subject(s) - mapk/erk pathway , p38 mitogen activated protein kinases , western blot , cell culture , cytokine , nf κb , interleukin 8 , interleukin 33 , interleukin , microbiology and biotechnology , immunology , biology , inflammation , kinase , biochemistry , gene , genetics
Background: Prominent infiltration of eosinophils into the airway mucosa and release of inflammatory mediators upon their adhesion onto airway epithelial cells are the immunopathogical mechanisms of allergic asthma. Objective: We investigated the effect of normal and paraformaldyhyde‐fixed human eosinophils on BEAS‐2B cells, a human bronchial epithelial cell line, for the release of inflammatory cytokine interleukin (IL)‐6. Methods: Interleukin‐6 in cell culture supernatant, protein amount of p38 mitogen‐activated protein kinase (MAPK), and nuclear factor‐ κ B (NF‐ κ B) activity in BEAS‐2B cells were analyzed by Western blot and enzyme‐linked immunosorbent assay (ELISA). IL‐6 gene expression was assessed by reverse transcriptase‐polymerase chain reaction (RT‐PCR), and p38 MAPK activity and inhibitor (I) κ B‐ α induction were evaluated by Western blot. Results: Co‐culture of BEAS‐2B cells and eosinophils induced a significant elevation of IL‐6 expression in BEAS‐2B cells. Interaction of eosinophils and BEAS‐2B cells led to a marked induction in phospho‐p38 MAPK, phospho‐I κ B‐ α and activity of NF‐ κ B in BEAS‐2B cells. NF‐ κ B inhibitor BAY 11‐7082 and p38 MAPK inhibitor SB 203580 significantly decreased IL‐6 release in a co‐culture of BEAS‐2B cells and eosinophils. Fixed human eosinophils were able to maintain their ability to induce IL‐6 release in co‐culture, activate p38 MAPK and NK‐ κ B, and up‐regulate IL‐6 gene expression in BEAS‐2B cells. Conclusions: These data indicate that the interaction of eosinophils and bronchial epithelial cells plays an important role in airway inflammation, at least partly, via IL‐6 induction.