Tritrichomonas foetus: Pathogenesis of acute infection in normal, estradiol-treated, and stressed mice

Rutkowski, Melanie R.; Harmsen, Allen G.

doi:10.1016/j.exppara.2006.07.009

Cited by 5 publications

(8 citation statements)

References 48 publications

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“…In T. foetus, severe infection is often associated with a large accumulation of neutrophils and macrophages, although it is still unclear how this response protects during the early colonization of the parasite. Rutkowski and Harmsen (2007) examined the effects of an early host response on the initial colonization of T. foetus in the murine reproductive tract (C57BL/6). They observed that mice deficient in gp91phox (NOX2) and iNOS, and only iNOS, had substantially higher parasite burdens than unmodified control mice.…”

Section: Discussionmentioning

confidence: 99%

Exposure of Tritrichomonas foetus to sublethal doses of metronidazole induces a specific proinflammatory response in murine macrophages

Ceballos‐Góngora,

Torres‐Romero,

Arana‐Argáez

et al. 2023

J Eukaryotic Microbiology

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Tritrichomonas foetus is a flagellated parasite that primarily infects the reproductive tissues of livestock, causing bovine trichomoniasis. The cytoplasmic membrane of T. foetus contains various compounds that contribute to adherence, colonization, and pathogenicity. Metronidazole (MTZ) is the main treatment for trichomoniasis, but the emergence of drug‐resistant strains is a concern due to improper use and dosing. T. foetus infection induces inflammation, and macrophages are key players in the immune response. However, our understanding of the host's immune response to T. foetus is limited, and the specific mechanisms underlying these responses are not well understood. This study aimed to investigate the impact of T. foetus surface proteins from trophozoites cultured under different sublethal MTZ conditions (MTZ‐treated T. foetus MPs) on macrophage activation. By analyzing cytokine levels and gene expression in murine macrophages, we demonstrated that MTZ‐treated T. foetus MPs induce a specific proinflammatory response. MTZ‐treated T. foetus MPs‐exposed macrophages exhibited a higher NO and H2O2 production and overexpression of iNOS and NOX‐2 genes in comparison to untreated T. foetus. Additionally, MTZ‐treated T. foetus MPs triggered a significant induction of the proinflammatory cytokines IL‐1β, IL‐6, TNF‐α, and IFN‐γ, as well as the overexpression of the TLR4, MyD88, and NF‐κB genes on murine macrophages. The study aimed to unravel the immunological response and potential proinflammatory pathways involved in T. foetus infection and MTZ stress. Understanding the immune responses and mechanisms through which T. foetus surface proteins activate macrophages can contribute to the development of new therapeutic strategies for controlling bovine trichomoniasis.

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Section: Discussionmentioning

confidence: 99%

Exposure of Tritrichomonas foetus to sublethal doses of metronidazole induces a specific proinflammatory response in murine macrophages

Ceballos‐Góngora,

Torres‐Romero,

Arana‐Argáez

et al. 2023

J Eukaryotic Microbiology

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“…Indeed, neutrophil numbers were increased in estrogen-treated and stressed T. foetus-infected mice over controls in a recent study. 55 Cows do not have a similar neutrophilic wave, although they do have a brief postestrual period of endometrial hemorrhage. Presumably, T. foetus organisms may be exposed to neutrophils from the systemic circulation during the flow of a negligible volume of blood during this time, but the relative numbers are likely less than those seen in the vaginal infiltrate of mice.…”

Section: Discussionmentioning

confidence: 99%

“…66 In fact, these interactions can be contradictory, as illustrated by a recent study of the effects of estrogen treatment on the immune response of T. foetus-infected mice, which showed that estrogen enhanced the inflammatory response and tissue damage but decreased the ability of T. foetus to establish infection. 55 Immune function and resistance to T. foetus infection may be compromised when estrogen levels are either too high or too low. It is also possible that, in these prepubertal mice, the vagina was infected and T. foetus organisms were established deep in the epithelial folds before the first diestrus resulted in a massive influx of neutrophils into the lumen.…”

Section: Discussionmentioning

confidence: 99%

“…Estrogen has been shown to have marked immune-modulating effects, both systemically and in the reproductive tract. 29,39,47,48,55,61,62 A recent mouse model demonstrated marked suppression of vaginal immunoglobulin (Ig) A, uterine IgG, and serum IgG in estrogenized CD1 mice compared with nonestrogenized mice, although a similar effect was not seen in BALB/c mice. 42 Estrogen's modulatory effect on eosinophils is particularly noteworthy 47 in light of the large number of eosinophils seen in T. foetus infections.…”

mentioning

confidence: 99%

“…23 More recently, mouse models that did not require estrogen supplementation were used to examine antibody responses to T. foetus infection in mice and adherence to reproductive mucosa in vivo. 40,42 Another mouse study examined the effects of stress and estrogens on infection, 55 but the effects on pregnancy were not examined in these models.…”

mentioning

confidence: 99%

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A Pregnant Mouse Model for BovineTritrichomonas foetusInfection

et al. 2008

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Abstract. The economically important effects of Tritrichomonas foetus infection in cattle are abortion and infertility, yet there has not been an animal model to examine the parasite-host interactions during gestation. In this study, 5-and 7-to 8-week-old BALB/cAnNCr, BALB/cJ, and SCID/NCr mice on a BALB/c background were intravaginally infected with T. foetus. All BALB/ cAnNCr and BALB/cJ mice, and 89% of SCID/NCr mice sustained infections for 13 weeks, if inoculated before 5 weeks of age. Infection rates were lower in all mouse strains inoculated at 7 weeks of age, although BALB/cAnNCr mice were significantly more susceptible than BALB/cJ or SCID/ NCr mice. Vaginal bacterial flora did not account for the variation in mouse-strain susceptibility, although coagulase-negative staphylococci in vaginal flora were associated with failure of T. foetus to infect. As with infected cattle, T. foetus-specific vaginal immunoglobulin (Ig) G and IgA antibodies were elevated after infection. The number and viability of day-10 fetuses were reduced in mice infected at 5 weeks of age and bred 12 weeks after infection. Lesions in pregnant and nonpregnant infected mice, including suppurative and eosinophilic vaginitis; cervicitis; endometritis with distension of the uterine lumen; endometrial ulceration; and glandular ectasia, with neutrophils in the glandular lumen and loss of gland epithelium, were similar to those in cattle. The decidua and placenta were multifocally necrotic. Immunohistochemistry demonstrated trichomonads in vaginal folds and uterine glands, and adjacent to fetal tissues. In summary, experimentally infected BALB/cAnNCr mice showed many pathologic similarities to cattle and may serve as a model to study host-trichomonad interactions.

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