Trichomonas vaginalis: Reactive oxygen species mediates caspase-3 dependent apoptosis of human neutrophils

Delayed Human Neutrophil Apoptosis by Trichomonas vaginalis Lysate

“…At the site of trichomoniasis, clearance of aged or apoptotic neutrophils may help to protect normal tissues from the toxic molecules released by necrotic neutrophils. Our previous study suggested that live T. vaginalis increases neutrophil apoptosis; this may contribute to the resolution of inflammation via clearance of apoptotic neutrophils [12,13]. However, the T. vaginalis lysate used in this experiment decreases neutrophil apoptosis and may subsequently allow the initiation of inflammation.…”

“…Since live T. vaginalis induced neutrophil apoptosis via Mcl-1 and caspase-3 in our previous studies, we decided to examine Mcl-1 and caspase-3 in neutrophils to investigate the related mechanism of T. vaginalis lysate-induced delayed neutrophil apoptosis [12,13]. As shown in sate-co-incubated neutrophils was maintained after 25 hr of incubation and at the same time point caspase-3 cleavage was reduced compared with untreated neutrophils.…”

“…In our previous report, live T. vaginalis induced human neutrophil apoptosis via a caspase-3 and Mcl-1 dependent manner using reactive oxygen species (ROS) [12,13]. However, the relationship between T. vaginalis lysate and the apoptosis of human neutrophils is still unclear.…”

“…The membrane potential of mitochondria is known to be decreased in neutrophils during apoptosis [13]. To determine whether T. vaginalis lysate induces a delay of neutrophil apoptosis via a mitochondrial pathway, change of the MMP was observed with a JC-1 probe.…”

“…Alteration of JC-1 aggregates (high MMP) and JC-1 monomers (low MMP) were measured using flow cytometry (FACSCalibur, Becton Dickinson, Heidelberg, Germany), and neutrophils with a low MMP were regarded as apoptotic neutrophils [13,18]. Surface CD16 receptor shedding was also used as a marker of neutrophil apoptosis [19].…”