Infection and Activation of Airway Epithelial Cells byChlamydia pneumoniae
Open Access
- 1 December 2000
- journal article
- Published by Oxford University Press (OUP) in The Journal of Infectious Diseases
- Vol. 182 (6) , 1678-1687
- https://doi.org/10.1086/317608
Abstract
The activation of primary human airway epithelial cells (HAECs) and of the bronchial epithelial cell line BEAS-2B by Chlamydia pneumoniae, an important respiratory pathogen, was characterized. A time-dependent enhanced release of interleukin (IL)—8 and prostaglandin-E2 and an increased expression of the epithelial adhesion molecule intercellular adhesion molecule—1 (ICAM-1), followed by subsequent transepithelial migration of polymorphonuclear neutrophils (PMN), were also demonstrated. The transepithelial PMN migration could be blocked by an anti—ICAM-1 monoclonal antibody (MAb) but not by MAbs against IL-8. In addition, there was an enhanced C. pneumoniae—mediated activation of NF-κB within 30–60 min in HAECs and BEAS-2B, which was followed by increases in mRNA synthesis of IL-8, ICAM-1, and cyclooxygenase-2, with maximal effects occurring 2 h after infection. Thus, C. pneumoniae infects and activates HAECs and BEAS-2B and therefore may be able to trigger a cascade of pro- and anti-inflammatory reactions during chlamydial infections.Keywords
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