Diesel exhaust particles increase IL-1β-induced human β-defensin expression via NF-κB-mediated pathway in human lung epithelial cells |
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| Authors: | Hae Yun Nam Eun-Kyung Ahn Hyung Jung Kim Young Lim Chun Beoun Lee Kyo Young Lee Val Vallyathan |
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| Affiliation: | (1) Catholic Neuroscience Center, The Catholic University of Korea, Seoul, 137–701, Korea;(2) Department of Occupational & Environmental Medicine, St. Mary's Hospital, The Catholic University of Korea, Seoul, 150–713, Korea;(3) Department of Internal Medicine, Yonsei University College of Medicine, Seoul, 135–270, Korea;(4) Environmental Parts R & D Center, Korea Automotive Technology Instititute, Cheonan, 330–912, Korea;(5) Department of Hospital Pathology, Kangnam St. Mary's Hospital, The Catholic University of Korea, Seoul, 137–701, Korea;(6) Exposure Assessment Branch and Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV, USA |
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| Abstract: | Background Human β-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 interleukin-1 beta (IL-1β)-stimulated A549 cells. |
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