Chlamydia trachomatis-induced apoptosis occurs in uninfected McCoy cells late in the developmental cycle and is regulated by the intracellular redox state.
Infections with the obligate intracellular bacterium Chlamydia trachomatis are characterized by avoidance of fusion between chlamydia-containing endosomes and lysosomes, bacterial persistence and development of post-infectious sequelae. In this report we show that C. trachomatis induces apoptosis in McCoy and HeLa cells. Apoptosis was monitored by three different techniques; enzyme-linked immunoassay (EIA) of fragmented nucleosomes, terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) and flow cytometry of propidium iodide-stained cells. Apoptosis occurred in uninfected cells, was induced late in the chlamydial developmental cycle, beyond 24 h post-infection and was dependent on bacterial protein synthesis. Apoptosis was not significantly increased in infected, inclusion-containing cells. Treatment of cells with the antioxidants ascorbic acid (10 microM) and alpha-tocopherol (10 microM) reduced the degree of apoptosis. These results suggest that host cells infected with C. trachomatis generate proapoptotic stimuli that induce apoptosis in uninfected, neighbouring cells and that the redox state of the cell is a regulator in chlamydia-induced apoptosis.
Schöier
J
J
Division of Clinical Microbiology, Faculty of Health Sciences, Linköping, Sweden.
Ollinger
K
K
Kvarnström
M
M
Söderlund
G
G
Kihlström
E
E
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis; D001426:Bacterial Proteins / Q000096:biosynthesis; D002460:Cell Line; D002692:Chlamydia trachomatis / Q000472:pathogenicity*; D006801:Humans; D020287:In Situ Nick-End Labeling; D051379:Mice; D010084:Oxidation-Reduction; D017382:Reactive Oxygen Species
D000975:Antioxidants; D001426:Bacterial Proteins; D017382:Reactive Oxygen Species