Chlamydia trachomatis serovar L2 infection model using human lymphoid Jurkat cells.

Kubo T et al 1 Chlamydia trachomatis serovar L2 infection model using human lymphoid Jurkat cells

Murine cytotoxic T lymphocytes induced following Chlamydia trachomatis intraperitoneal or genital tract infection respond to cells infected with multiple serovars.

The obligate intracellular bacterium Chlamydia trachomatis is associated with human diseases ranging from blinding trachoma to sexually acquired genital infections and the systemic disease lymphogranuloma venereum (LGV). We have previously reported the isolation and culture of protective murine cytotoxic T lymphocytes (CTL) following intraperitoneal infection with C. trachomatis serovar L2, a s...

Binding, ingestion, and multiplication of Chlamydia trachomatis (L2 serovar) in human leukocyte cell lines.

We examined the ability of lymphoblastoid-myeloid cell lines to bind, ingest, and permit multiplication of Chlamydia trachomatis (L2 serovar). Four types of chlamydia-cell line interactions were observed: minimal bacterial binding; bacterial binding, followed by ingestion and high-level multiplication; bacterial binding, followed by ingestion but minimal multiplication; and bacterial binding, b...

Chlamydia pneumoniae uses the mannose 6-phosphate/insulin-like growth factor 2 receptor for infection of endothelial cells.

Several mechanisms for attachment and entry of Chlamydia have been proposed. We previously determined that the major outer membrane protein of Chlamydia trachomatis is glycosylated with a high-mannose oligosaccharide, and a similar structure inhibited the attachment and infectivity of C. trachomatis in epithelial cells. Because insulin-like growth factor 2 (IGF2) was shown to enhance the infect...

Chlamydia trachomatis induces remodeling of the actin cytoskeleton during attachment and entry into HeLa cells.

To elucidate the host cell machinery utilized by Chlamydia trachomatis to invade epithelial cells, we examined the role of the actin cytoskeleton in the internalization of chlamydial elementary bodies (EBs). Treatment of HeLa cells with cytochalasin D markedly inhibited the internalization of C. trachomatis serovar L2 and D EBs. Association of EBs with HeLa cells induced localized actin polymer...