Study of the uterine local immune response in a murine model of embryonic death due to Tritrichomonas foetus

WOUDWYK M; MONTEAVARO C; JENSEN F; SOTO P; BARBEITO C; ZENCLUSSEN AC

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY

WILEY-BLACKWELL PUBLISHING, INC

Año: 2012 vol. 68 p. 128 - 137

1046-7408

Los dos ultimos autores trabajaron en igual medida ProblemBovine tritrichomonosis is a sexually transmitted disease caused byTritrichomonas foetus, characterized by conceptus loss. We developed amouse model of tritrichomonosis to study the mechanisms involved inthe embryonic death. We hypothesized that embryonic death may bedue to an exacerbated maternal response to the pathogen that thenaffects embryo development.Method of studyWe infected BALB/c mice with Tritrichomonas foetus and paired themafter confirming active infection. We studied the expression of pro- andanti-inflammatory cytokines, markers for T regulatory and T helper 17cells as well as haem-oxygenase-1 expression in uterine tissue by realtimeRT-PCR.ResultsAs expected, TNF-a was augmented in infected animals. IL-10 and IL-4were also up-regulated. Treg-associated genes were higher expressed inuteri of infected group. In mice that have lost their conceptus after theinfection, haem-oxygenase-1 (HO-1) mRNA levels were stronglydecreased, while RORct mRNA, a reliable marker for Th17, was aug-mented in uterus.ConclusionA T effector response of type 1 and 17 may be involved in tritrichomo-nosis-related embryonic death. This alters protective mechanisms asHO-1. Increased regulatory T cells may facilitate embryonic death bypromoting the persistence of infection.