Chlamydia trachomatis does not bind to alpha beta 1 integrins to colonize a human endometrial epithelial cell line cultured in vitro.

Chlamydia trachomatis is the leading cause of bacterially acquired sexually transmitted diseases in the United States and Europe. As an obligate intracellular pathogen, this bacterium must invade epithelial cells in order to survive and grow. Thus, multiple strategies probably exist for initial binding of chlamydiae to their target cells. Since a variety of bacteria have exploited integrins to colonize tissues, and a precedent existed for the involvement of extracellular matrix components in chlamydial attachment, this study first analyzed, by flow cytometry, integrins expressed by the human endometrial epithelial cell line HEC-1B. The genital cells were then exposed to monoclonal antibodies directed against those integrins and assayed for chlamydial attachment and inclusion development. Monoclonal antibodies bound to the alpha and/or beta 1 subunit of classic integrin receptors displayed by HEC-1B cells were not able to prevent colonization and infection of the epithelial cells by a genital isolate of C. trachomatis.