The ciliary activity of ciliated bronchial epithelial cells was studied after infection with Chlamydia pneumoniae (strain TW-183) and Chlamydia trachomatis (biovar L2 [434/Bu]). C. pneumoniae, known to cause respiratory infections, had a marked ciliastatic effect, completely aborting ciliary motion within 48 h. This effect was not inhibited by inactivation of C. pneumoniae elementary bodies (EBs) by UV irradiation. In contrast, inactivation of EBs by heat (56 degrees C, 30 min) or by rabbit-specific immune sera to TW-183 antigen blocked the ciliastatic effect induced by C. pneumoniae infection. The effect of C. pneumoniae was specific. C. trachomatis, which causes sexually transmitted disease, did not block ciliary motion by 48 h after infection. A decrease in ciliary activity of ciliated bronchial cells produced by C. pneumoniae can contribute to both initiation and pathogenesis of respiratory infections induced by this pathogen.