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Study of the Uterine Local Immune Response in a Murine Model of Embryonic Death Due to Tritrichomonas foetus
Author(s) -
Woudwyk Mariana A.,
Monteavaro Cristina E.,
Jensen Federico,
Soto Pedro,
Barbeito Claudio G.,
Zenclussen Ana C.
Publication year - 2012
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.2012.01159.x
Subject(s) - tritrichomonas foetus , conceptus , biology , embryonic stem cell , immune system , embryo , immunology , andrology , fetus , effector , embryogenesis , uterus , proinflammatory cytokine , endometrium , inflammation , microbiology and biotechnology , pregnancy , gene , endocrinology , medicine , genetics
Problem 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. Method of study 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 ROR γt mRNA , a reliable marker for T h17, was augmented in uterus. Conclusion 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.