Study of the Uterine Local Immune Response in a Murine Model of Embryonic Death Due to <i>Tritrichomonas foetus</i>

Woudwyk, Mariana A.; Monteavaro, Cristina Esther; Jensen, Federico; Soto, Pedro; Barbeito, Claudio Gustavo; Zenclussen, Ana Claudia

doi:10.1111/j.1600-0897.2012.01159.x

Cited by 11 publications

(13 citation statements)

References 44 publications

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“…In previous studies of T. foetus infection during early pregnancy, we have found changes in the local immune response at the maternal-fetal interface (Woudwyk et al, 2012), as well as in the expression of uterine epithelial carbohydrates (Woudwyk et al, 2013). These changes and the here reported allow us to support the hypothesis of the abortion as a multifactorial process.…”

Section: Discussionsupporting

confidence: 85%

Apoptosis and cell proliferation in the mouse model of embryonic death induced by Tritrichomonas foetus infection

Woudwyk

Zanuzzi

Nishida

et al. 2015

Experimental Parasitology

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Section: Discussionsupporting

confidence: 85%

Apoptosis and cell proliferation in the mouse model of embryonic death induced by Tritrichomonas foetus infection

Woudwyk

Zanuzzi

Nishida

et al. 2015

Experimental Parasitology

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“…During pregnancy, intrauterine infections begin in the decidua, extend to the amnion and chorion and finally reach the amniotic cavity and the fetus (13). Bacteria gain access to gestational tissues through one of three major routes: by ascending into the uterus from the lower tract, descending into the uterus from the peritoneal cavity or via the maternal circulation (14) (6). Bacterial infections that ascend from the lower FRT are the most common route of uterine infection, and it is not known why some women suffer such infections that threaten pregnancies and fetal survival (15).…”

Section: Introductionmentioning

confidence: 99%

Viral Infection of the Pregnant Cervix Predisposes to Ascending Bacterial Infection

Racicot

Cardenas

Wünsche

et al. 2013

The Journal of Immunology

146

135

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Preterm birth is the major cause of neonatal mortality and morbidity, and bacterial infections that ascend from the lower female reproductive tract (FRT) are the most common route of uterine infection leading to preterm birth. The uterus and growing fetus are protected from ascending infection by the cervix, which controls and limits microbial access by the production of mucus, cytokines and anti-microbial peptides (AMPs). If this barrier is compromised, bacteria may enter the uterine cavity leading to preterm birth. Using a mouse model, we demonstrate, for the first time, that viral infection of the cervix, during pregnancy, reduces the capacity of the FRT to prevent bacterial infection of the uterus. This is due to differences in susceptibility of the cervix to infection by virus during pregnancy and the associated changes in TLR and AMP expression and function. We suggest that preterm labor is a polymicrobial disease, which requires a multifactorial approach for its prevention and treatment.

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“…Molecular expression of pro-inflammatory cytokines, markers for T regulatory and T helper 17 cells, as well as heme oxygenase-1 expression in uterine tissue of BALB/c mice has demonstrated TNF-α augmentation in the uterus of infected animals. Anti-inflammatory cytokine IL-10 was also upregulated (Vilela and Benchimol 2013;Woudwyk et al 2012). These studies provide new hope for development of vaccines against trichomoniasis.…”

Section: Immunization In Humansmentioning

confidence: 76%

Comparative aspects of immunity and vaccination in human and bovine trichomoniasis: a review

Chapwanya

Usman

Irons

2015

Trop Anim Health Prod

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Trichomonas vaginalis and Tritrichomonas foetus are important extracellular protozoans that cause, respect i v e l y, h u m a n a n d b o v i n e v e n e r e a l d i s e a s e s . Trichomonads are extracellular parasites that primarily inhabit the genital tracts of the mammalian hosts where they overcome the mucus barrier and parasitize mucosa by contact-dependent or contact-independent cytotoxicity. Transient immunity is usually achieved by the host after clinical infection. At present, vaccination in cattle reduces infection rates and reproductive wastage in affected herds. After vaccination, immunoglobulin G (IgG) levels increase in systemic circulation while immunoglobulin A (IgA) levels rise in the vagina. Only moderate protection is conferred by means of vaccination. Future vaccine development strategies are needed for cattle to enhance the antigenic component or use adjuvant that strongly activates the innate immune response to produce safe and potent vaccines. This paper reviews the current knowledge of the immunology of trichomoniasis infection and the challenges and potential of vaccines in the control of the infection in human and bovine trichomoniasis.

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Study of the Uterine Local Immune Response in a Murine Model of Embryonic Death Due to Tritrichomonas foetus

Abstract: 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.

Cited by 11 publications

References 44 publications

Apoptosis and cell proliferation in the mouse model of embryonic death induced by Tritrichomonas foetus infection

Apoptosis and cell proliferation in the mouse model of embryonic death induced by Tritrichomonas foetus infection

Viral Infection of the Pregnant Cervix Predisposes to Ascending Bacterial Infection

Comparative aspects of immunity and vaccination in human and bovine trichomoniasis: a review

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