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Neutrophil elastase up‐regulates human β‐defensin‐2 expression in human bronchial epithelial cells
Author(s) -
Griffin Siobhan,
Taggart Clifford C.,
Greene Catherine M.,
O'Neill Shane,
McElvaney Noel G.
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)00577-5
Subject(s) - microbiology and biotechnology , defensin , beta defensin , elastase , neutrophil elastase , cell culture , gene expression , tumor necrosis factor alpha , flow cytometry , interleukin 8 , biology , lipopolysaccharide , chemistry , cytokine , gene , inflammation , immunology , enzyme , biochemistry , genetics
Human β‐defensin‐2 (HBD‐2) gene expression is induced by tumour necrosis factor‐α, interleukin‐1β and lipopolysaccharide. The objective of this study was to investigate the effect of neutrophil elastase (NE), a major pro‐inflammatory protease, on HBD‐2 expression. HBD‐2 gene expression was assessed by reverse transcription polymerase chain reaction in the human bronchial epithelial cell line 16HBE14o− and primary normal human bronchial epithelial (NHBE) cells. Optimal HBD‐2 expression was induced with 100 nM NE. Using a HBD‐2‐luciferase reporter construct, luciferase activity increased significantly in 16HBE14o− cells following incubation with NE. An increase in HBD‐2 protein expression was observed in primary NHBE cells after incubation with NE as assessed by laser scanning cytometry. In conclusion, NE up‐regulates HBD‐2 expression in bronchial epithelial cells.