Study of the uterine local immune response in a murine model of embryonic death due to Tritrichomonas foetus.
OBJECTIVE
Bovine tritrichomonosis is a sexually transmitted disease caused by Tritrichomonas foetus, characterized by conceptus loss. We developed a mouse model of tritrichomonosis to study the mechanisms involved in the embryonic death. We hypothesized that embryonic death may be due to an exacerbated maternal response to the pathogen that then affects embryo development.


METHODS
We infected BALB/c mice with Tritrichomonas foetus and paired them after confirming active infection. We studied the expression of pro- and anti-inflammatory cytokines, markers for T regulatory and T helper 17 cells as well as haem-oxygenase-1 expression in uterine tissue by real-time RT-PCR.


RESULTS
As expected, TNF-α was augmented in infected animals. IL-10 and IL-4 were also up-regulated. Treg-associated genes were higher expressed in uteri of infected group. In mice that have lost their conceptus after the infection, haem-oxygenase-1 (HO-1) mRNA levels were strongly decreased, while RORγt mRNA, a reliable marker for Th17, was augmented in uterus.


CONCLUSIONS
A T effector response of type 1 and 17 may be involved in tritrichomonosis-related embryonic death. This alters protective mechanisms as HO-1. Increased regulatory T cells may facilitate embryonic death by promoting the persistence of infection.
Laboratory of Histology and Embryology, Faculty of Veterinary Sciences, National University of La Plata, La Plata, Buenos Aires, Argentina.
Mariana A
MA
Woudwyk
Cristina E
CE
Monteavaro
Federico
F
Jensen
Pedro
P
Soto
Claudio G
CG
Barbeito
Ana C
AC
Zenclussen
D000818:Animals; D002417:Cattle; D002478:Cells, Cultured; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D020964:Embryo Loss / Q000276:immunology* / Q000469:parasitology*; D005260:Female; D051547:Heme Oxygenase-1 / Q000235:genetics / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D011247:Pregnancy; D015597:Pregnancy Complications, Parasitic / Q000209:etiology / Q000276:immunology*; D011528:Protozoan Infections / Q000150:complications*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D058504:Th17 Cells / Q000276:immunology; D016835:Tritrichomonas foetus; D014599:Uterus / Q000276:immunology* / Q000469:parasitology
D016207:Cytokines; D018836:Inflammation Mediators; D051547:Heme Oxygenase-1