Placental Pathology Associated with Fetal Death in Cattle Inoculated with Neospora caninum by Two Different Routes in Early Pregnancy

Macaldowie, C.; Maley, S.W.; Wright, Steve; Bartley, Paul M.; Esteban-Redondo, I.; Buxton, D.; Innes, Elisabeth A.

doi:10.1016/j.jcpa.2004.02.005

Cited by 88 publications

(126 citation statements)

References 27 publications

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“…Local or systemic chemokine dysregulation could conceivably contribute to the placental phenotypes observed at E14 in Ackr2-deficient DBA/1j mice, by, for example, altering leukocyte recruitment into the placenta. Excessive or uncontrolled inflammation within the placenta can compromise its function and has been well documented to cause fetal loss in both animals and humans (56)(57)(58)(59), and the CCL2/CCR2 axis has been implicated in preeclampsia (60), the regulation of Th2 responses at the fetomaternal interface (18,61), the recruitment of Th17 cells into the decidua (24), and the promotion of decidual stromal cell growth (62). Preliminary quantitative real-time PCR and histology have failed to provide evidence that Ackr2 deficiency modulates leukocyte abundance in the E14 placenta (data not shown), but further comparative analysis of immune cells in WT and Ackr2-deficient placentas throughout gestation could provide insight into the cellular basis for the placental defects arising from Ackr2 loss.…”

Section: Discussionmentioning

confidence: 99%

Atypical Chemokine Receptor ACKR2 Mediates Chemokine Scavenging by Primary Human Trophoblasts and Can Regulate Fetal Growth, Placental Structure, and Neonatal Mortality in Mice

Teoh

Menzies

Hansell

et al. 2014

The Journal of Immunology

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Inflammatory chemokines produced in the placenta can direct the migration of placental leukocytes using chemokine receptors that decorate the surface of these cells. Fetal trophoblasts can also express receptors for inflammatory chemokines, and they are one of the few cell types that express atypical chemokine receptor 2 (ACKR2), previously known as D6. ACKR2 binds many inflammatory CC chemokines but cannot stimulate cell migration or activate signaling pathways used by conventional chemokine receptors. Existing evidence suggests that ACKR2 is a specialized chemokine scavenger, but its function in primary human trophoblasts has not been explored. In mice, ACKR2 is thought to be dispensable for the reproductive success of unchallenged females that have conceived naturally, but it can suppress inflammation-induced abortion and aid the survival of implanted allogeneic embryos. In this article, we demonstrate that cultured primary human trophoblasts express ACKR2 far more strongly than genes encoding conventional receptors for inflammatory CC chemokines. Moreover, these cells are capable of the rapid internalization and efficient scavenging of extracellular chemokine, and this is mediated by ACKR2. We also report that in unchallenged DBA/1j mice, Ackr2 deficiency increases the incidence of stillbirth and neonatal death, leads to structural defects in the placenta, and can decrease fetal weight. Loss of Ackr2 specifically from fetal cells makes a key contribution to the placental defects. Thus, primary human trophoblasts use ACKR2 to scavenge chemokines, and ACKR2 deficiency can cause abnormal placental structure and reduced neonatal survival.

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Section: Discussionmentioning

confidence: 99%

Atypical Chemokine Receptor ACKR2 Mediates Chemokine Scavenging by Primary Human Trophoblasts and Can Regulate Fetal Growth, Placental Structure, and Neonatal Mortality in Mice

Teoh

Menzies

Hansell

et al. 2014

The Journal of Immunology

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“…Trafficking of leukocytes to disseminate intracellular parasites via a Trojan horse-type mechanism has been postulated for other apicomplexan parasites, such as Toxoplasma gondii [17]. At present, N. caninum DNA has been found in the white cell fraction of blood in naturally [18] and experimentally [19] infected cows. In addition, N. caninum antiserum has been found to bind to phagocytes [20] and the related coccidian, T. gondii, has been demonstrated to be resistant to lysis after internalization by macrophages [21].…”

Section: Discussionmentioning

confidence: 99%

Experimental neosporosis in bulls: Parasite detection in semen and blood and specific antibody and interferon-gamma responses

et al. 2007

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Aim: To investigate the presence of Neospora caninum in semen and blood, and the development of specific antibody and interferon-gamma (IFN-g) responses in experimentally infected bulls. Methods: Eight bulls were intravenously infected with 10 8 live N. caninum tachyzoites of NC-1 isolate. The presence of N. caninum in semen and blood was assessed using a nested-PCR procedure. PCR-positive semen samples were bioassayed using a BALB/c nu/nu mouse model. Specific anti-N. caninum antibody and IFN-g responses were also examined. In parallel, eight seronegative bulls were studied as non-infected controls. All bulls were monitored for 26 weeks. Results: All eight experimentally infected bulls showed N. caninum DNA in their semen and/or blood samples at some time during the course of the study. Parasite load in semen ranged from 0.1 to 14.5 parasites/ml (mean 6.0). N. caninum could not be detected in BALB/c nu/nu mice inoculated with PCR-positive semen samples. A significant increase in mean serum specific IgM antibody response to N. caninum was detected between 10 and 28 days post-infection (p.i.). Serum specific IgG, IgG1, and IgG2 antibody levels in experimentally infected bulls were significantly different after 21, 10, and 14 days p.i. as compared to controls, respectively. Specific anti-N. caninum IgG were detected in seminal plasma from infected bulls and values obtained were different from controls after 25 days p.i. Mean specific IFN-g responses in experimentally infected bulls were significantly higher than controls 3 days p.i. Conclusions: This is the first study to report the presence of N. caninum DNA in the semen and blood of experimentally infected bulls. Our observations indicate an intermittent presence of N. caninum in low numbers in semen and associated with chronic stage of the infection. This study is also the first to report the detection of anti-N. caninum IgG in seminal plasma of experimentally infected bulls. #

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“…Our findings show that these areas are most useful for evaluating the extent of N. caninum infection, investigating the pathogenesis of neosporosis, and evaluating antiparasitic drugs and vaccines against such organisms. Although the Nc-1 isolate has a lower ability for cyst formation, this isolate has been used in many studies of the pathogenesis of neosporosis and can induce fetal death in experimentally infected cattle (20)(21)(22). On the other hand, cystogenic isolates, such as Nc-Liv, may show some differences in brain parasite burdens and pathological changes.…”

mentioning

confidence: 99%

Tissue Distribution of Neospora caninum in Experimentally Infected Cattle

Nishimura

Kohara

Hiasa

et al. 2013

Clin Vaccine Immunol

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Placental Pathology Associated with Fetal Death in Cattle Inoculated with Neospora caninum by Two Different Routes in Early Pregnancy

Cited by 88 publications

References 27 publications

Atypical Chemokine Receptor ACKR2 Mediates Chemokine Scavenging by Primary Human Trophoblasts and Can Regulate Fetal Growth, Placental Structure, and Neonatal Mortality in Mice

Atypical Chemokine Receptor ACKR2 Mediates Chemokine Scavenging by Primary Human Trophoblasts and Can Regulate Fetal Growth, Placental Structure, and Neonatal Mortality in Mice

Experimental neosporosis in bulls: Parasite detection in semen and blood and specific antibody and interferon-gamma responses

Tissue Distribution of Neospora caninum in Experimentally Infected Cattle

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