Diesel exhaust particles increase IL-1beta-induced human beta-defensin expression via NF-kappaB-mediated pathway in human lung epithelial cells.

ABSTRACT:

Background

Human beta-defensin (hBD)-2, antimicrobial peptide primarily induced in epithelial cells, is a key factor in the innate immune response of the respiratory tract. Several studies showed increased defensin levels in both inflammatory lung diseases, such as cystic fibrosis, diffuse panbronchiolitis, idiopathic pulmonary fibrosis and acute respiratory distress syndrome, and infectious diseases. Recently, epidemiologic studies have demonstrated acute and serious adverse effects of particulate air pollution on respiratory health, especially in people with pre-existing inflammatory lung disease. To elucidate the effect of diesel exhaust particles (DEP) on pulmonary innate immune response, we investigated the hBD-2 and interleukin-8 (IL-8) expression to DEP exposure in interleuk

SUBMITTER: Nam HY 

PROVIDER: S-EPMC1524805 | biostudies-literature | 2006 May

REPOSITORIES: biostudies-literature