ACZ and CGB share senior authorship.
Study of the Uterine Local Immune Response in a Murine Model of Embryonic Death Due to Tritrichomonas foetus
Article first published online: 5 JUN 2012
© 2012 John Wiley & Sons A/S
American Journal of Reproductive Immunology
Volume 68, Issue 2, pages 128–137, August 2012
How to Cite
Woudwyk MA, Monteavaro CE, Jensen F, Soto P, Barbeito CG, Zenclussen AC. Study of the uterine local immune response in a murine model of embryonic death due to Tritrichomonas foetus. Am J Reprod Immunol 2012
- Issue published online: 12 JUL 2012
- Article first published online: 5 JUN 2012
- Manuscript Accepted: 23 APR 2012
- Manuscript Received: 13 MAR 2012
- German Research Council (DFG)
- ACZ (ZE 526 ⁄ 4-2)
- German Academic Exchange Service (DAAD)
- Bovine genital tritrichomonosis;
- embryonic death;
- Tritrichomonas foetus
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.
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.
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.