ISSN:
1398-9995
Quelle:
Blackwell Publishing Journal Backfiles 1879-2005
Thema:
Medizin
Notizen:
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-κB (NF-κB) 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)κB-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-IκB-α and activity of NF-κB in BEAS-2B cells. NF-κB 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-κB, 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.
Materialart:
Digitale Medien
URL:
http://dx.doi.org/10.1111/j.1398-9995.2005.00884.x
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