IMBECU   20882
INSTITUTO DE MEDICINA Y BIOLOGIA EXPERIMENTAL DE CUYO
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Disruption of ctl0175 hampers Chlamydia trachomatis replication post IFN- gamma-induced stress.
Autor/es:
PANZETTA, MARIA E.; DAMIANI, MARÍA T.; LUJAN, A.; VALDIVIA, RAPHAEL H.; BASTIDAS, ROBERT J.; SAKA, HÉCTOR A.
Lugar:
Paraná
Reunión:
Congreso; 54º Reunión Anual de la Sociedad Argentina de Investigación Bioquímica y Biología Molecular (SAIB); 2018
Institución organizadora:
Sociedad Argentina de Investigación Bioquímica y Biología Molecular
Resumen:
Chlamydia trachomatis (CT) is the most common sexually transmitted bacterial pathogen globally. CT causes asymptomatic, persistentinfections leading to serious complications, particularly in young women. CT is an obligate intracellular bacterium alternating between twodevelopmental forms: the infectious elementary body (EB) and the non-infectious, replicative reticulate body (RB). In presence of stressors suchas interferon-gamma (IFN), CT enters a viable but non-cultivable or ―persistent‖ state. Once the stressors are removed, CT resumes replicationand continues to propagate. In a high throughput screen to identify chlamydial genes involved in persistence, we previously found that nullmutations in ctl0175/ptr (encoding an uncharacterized hypothetical protease), lead to a significant decrease in the generation of infectiousprogeny after IFN-induced stress. In Chlamydia, this may be due to reduced genome replication or to blocked RB/EB differentiation. Wegenerated a ptr::GII (ptr knockout) strain and quantified the rate of genome accumulation during IFN-treatment and recovery, compared to thewild type L2 strain. We found that ptr::GII exhibits reduced genome replication during recovery post IFN-induced stress, indicating that ptr isrequired for engaging rapid exit of persistence and replication upon IFN removal. We used a female genital tract model of infection in mice andsurprisingly found increased chlamydial burden at 14 days post-infection for the ptr::GII strain. Overall, these results point that a reducedreplication rate upon IFN removal enhances the ability of this bacteria to establish a long-lasting infection in the uterus.