The activation of primary human airway epithelial cells (HAECs) and of the
bronchial epithelial cell line BEAS-2B by Chlamydia pneumoniae, an importan
t respiratory pathogen, was characterized. A time-dependent enhanced releas
e of interleukin (IL)-8 and prostaglandin-E-2 and an increased expression o
f the epithelial adhesion molecule intercellular adhesion molecule-1 (ICAM-
1), followed by subsequent transepithelial migration of polymorphonuclear n
eutrophils (PMN), were also demonstrated. The transepithelial PMN migration
could be blocked by an anti-ICAM-1 monoclonal antibody (MAb) but not by MA
bs against IL-8. In addition, there was an enhanced C. pneumoniae-mediated
activation of NF-kappaB within 30-60 min in HAECs and BEAS-2B, which was fo
llowed by increases in mRNA synthesis of IL-8, ICAM-1, and cyclooxygenase-2
, with maximal effects occurring 2 h after infection, Thus, C. pneumoniae i
nfects and activates HAECs and BEAS-2B and therefore may be able to trigger
a cascade of pro- and anti-inflammatory reactions during chlamydial infect
ions.