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Apoptosis and cell proliferation in the mouse model of embryonic death induced by Tritrichomonas foetus infection
•The cytopathic effect induced by Tritrichomonas foetus alters uterine epithelial kinetic.•Uterine cell death index is higher in infected mice that lost their conceptus.•Uterine cell proliferation rate is increased in T. foetus-infected animals.•Apoptosis participates in the pathogeny of the abortio...
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Published in: | Experimental parasitology 2015-09, Vol.156, p.32-36 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | •The cytopathic effect induced by Tritrichomonas foetus alters uterine epithelial kinetic.•Uterine cell death index is higher in infected mice that lost their conceptus.•Uterine cell proliferation rate is increased in T. foetus-infected animals.•Apoptosis participates in the pathogeny of the abortion during tritrichomonosis.•The increase in the cell proliferation may act as compensatory host response.
Bovine tritrichomonosis is a sexually transmitted disease caused by the protozoon Tritrichomonas foetus and characterised by embryonic-death and abortion. During pregnancy, the processes of cell proliferation and death play a crucial role for blastocyst implantation and the subsequent maintenance of early pregnancy, and their misbalance may lead to the abortion. In this study, we aimed to investigate whether cell proliferation and death may be altered during tritrichomonosis. For this purpose, we used pregnant BALB/c mice as an alternative experimental animal model that has successfully reproduced the infection. We analysed the immunohistochemical expression of active caspase-3 and proliferating cell nuclear (PCNA) antigens in the endometrium of infected mice. We found an increase in the number of caspase-3 positive cells in infected mice that were not pregnant at the necropsy. Besides, the number of positive proliferating cells increased in the uterine luminal epithelium of infected animals killed at 5–7 days post coitum (dpc). Pregnant infected mice killed at 8–11 dpc showed higher proliferation than control animals. We suggest that the cytopathic effect induced by T. foetus in the uteri of infected mice may induce the apoptosis of the epithelial cells and, as a result, promote a compensatory proliferative response. The information described here will be helpful to further study the pathogenesis of the bovine tritrichomonosis. |
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ISSN: | 0014-4894 1090-2449 |
DOI: | 10.1016/j.exppara.2015.05.013 |