Endotoxin-induced and prostaglandin-mediated effects on corpus luteum function in the mare

Fredriksson, G.; Kindahl, H.; Stabenfeldt, G. H.

doi:10.1016/0093-691x(86)90066-x

Cited by 26 publications

(15 citation statements)

References 10 publications

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“…Previous studies showed that exposure to Escherichia coli endotoxins contributed to the termination of pregnancy at any stage of gestation [14, 15], but little is known about the mechanisms involved. The possible mechanisms of LPS-induced abortion might be due to the secretion of tumor necrosis factor-alpha (TNF- α ) by triggered macrophages (M φ ), which act on placental blood vessels directly, resulting in hemorrhagic necrosis [16].…”

Section: Discussionmentioning

confidence: 99%

Quercetin and Bornyl Acetate Regulate T‐Lymphocyte Subsets and INF‐γ/IL‐4 Ratio In Utero in Pregnant Mice

Wang

Shi

et al. 2010

Evidence-Based Complementary and Alternative Medicine

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The objective of this study is to investigate the antiabortive effects of Quercetin and Bornvl Acetate and their immunological modulation at maternal-fetal interface. Lipopolysaccharide (LPS) was injected via tail vein to induce abortion in mice which received Quercetin and Bornvl Acetate at days 4–7 of gestation. Uterine CD4+/CD8+ T lymphocytes and IFN-γ/IL-4 of each group (n = 10) were detected by immunohistochemistry and enzyme-linked immunosorbent assay, respectively. The ratio of CD4+/CD8+ increased significantly (P < .01) in the uterus of LPS-induced abortion mice. In the Quercetin and Bornvl Acetate pretreated mice followed by LPS administration, the ratio of CD4+/CD8+ dropped to 0.562 ± 0.021, lower than that of LPS-abortion group (P < .01). The mean value of IFN-γ/IL-4 in LPS-treated mice was 0.310 ± 0.066, higher than that of Quercetin and Bornyl Acetate group. The results indicate that Quercetin and Bornyl Acetate have an antiabortive effect through modulation of immunological balance at maternal-fetal interface.

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Section: Discussionmentioning

confidence: 99%

Quercetin and Bornyl Acetate Regulate T‐Lymphocyte Subsets and INF‐γ/IL‐4 Ratio In Utero in Pregnant Mice

Wang

Shi

et al. 2010

Evidence-Based Complementary and Alternative Medicine

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“…For example, abortion in pregnant rodents following endotoxin administration is accompanied by severe damage to the placenta [25] and endometrium [26], yet in other species no recognized lesions accompany abortion or preterm delivery. In the goat [27], pig [28], horse [29], and cow [30][31][32], pregnancy loss is attributed to altered maternal endocrine function, most notably, regression of the corpus luteum followed by abortion or onset of preterm labor. In sheep and primates, however, maintenance of pregnancy toward the end of gestation is placenta-dependent, and a functional corpus luteum is not required.…”

Section: Discussionmentioning

confidence: 99%

Effect of Salmonella Endotoxin Administered to the Pregnant Sheep at 133–142 Days Gestation on Fetal Oxygenation, Maternal and Fetal Adrenocorticotropic Hormone and Cortisol, and Maternal Plasma Tufnor Necrosis Factor α Concentrations1

Schlafer

Yuh

Foley

et al. 1994

Biology of Reproduction

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We studied the effects of maternal exposure to endotoxin on pregnancy outcome, stimulation of the hypothalamo-hypophyseal-adrenal axes (HHAA) of ewes and their fetuses, and maternal production of tumor necrosis factor alpha (TNF alpha), a central mediator in the pathogenesis of bacterial endotoxemia. Either endotoxin (lipopolysaccharide, LPS) from Salmonella typhimurium or saline was administered to pregnant sheep (n = 10) at 137.6 +/- 3.5 days gestational age by slow i.v. infusion at 1 microgram.kg-1 total dose over a 3-h period. Fetuses of ewes treated with LPS became hypoxemic by 2.5 h after initiation of LPS infusion. Maternal ACTH increased and peaked during LPS administration to levels approximately 10-fold greater in treated than in control ewes. In contrast, fetal ACTH levels were maximum at 6-12 h. Maternal and fetal cortisol levels were significantly different from control levels by 1 and 12 h, respectively. Maternal plasma TNF alpha peaked (6-7-fold over baseline) at 1-2 h after initiation of LPS administration and steadily declined over the following 48 h. Four of 5 treated ewes either delivered or their fetuses died within 28 h. In summary, infusion of LPS caused fetal hypoxemia and stimulated both fetal and maternal HHAA followed by preterm labor by 28 h after infusion in 4 of 5 ewes. Three of the fetuses died in utero. Maternal plasma TNF alpha rose rapidly, but the specific role it may play in initiation of preterm labor remains to be elucidated.

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“…Endotoxin-induced pregnancy losses associated with embryonic death, abortion, preterm labor and delivery have been documented in a number of species (Edqvist et al 1984, Fredriksson et al 1986, Giri et al 1990, Schlafer et al 1994. However, the mechanism of LPS-induced abortion is poorly understood.…”

Section: Discussionmentioning

confidence: 99%

A ‘minimum dose’ of lipopolysaccharide required for implantation failure: assessment of its effect on the maternal reproductive organs and interleukin-1α expression in the mouse

Deb¹,

Chaturvedi²,

Jaiswal³

2004

Reproduction

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Genital tract infections caused by gram-negative bacteria induce abortion and are one of the most common complications of human pregnancy. This study was carried out to decipher the mechanism of gram-negative bacterial lipopolysaccharide (LPS)-induced pregnancy loss, using a mouse (Park strain) model. Since many of the biological effects of LPS are mediated by interleukin (IL)-1a, the role of IL-1a in LPS-induced pregnancy loss was studied. Pregnant female animals were injected intraperitoneally (i.p.) with different doses (1 to 50 mg) of LPS from Salmonella minnesota Re-595, on day 0.5 of pregnancy. We found that 250 mg/kg body weight (i.e. 5 mg/female mouse) of LPS when given on day 0.5 of pregnancy was the 'minimum dose' (MD) required to completely inhibit the implantation of the blastocyst in the mouse. The effect of this dose on the pathophysiology of the various reproductive organs (i.e. uterus, ectoplacental cones, developing fetus, ovaries etc.) was assessed on day 14 of pregnancy. The effects of this dose on the level and pattern of expression of the proinflammatory cytokine IL-1a in the maternal uterine horns and preimplantation stage embryos were studied by RT-PCR. A single dose (100 ng/mouse) of recombinant mouse IL-1a was given i.p. to pregnant females on day 1 of pregnancy to study its effect on implantation. Our results show that treatment of the pregnant animals with LPS may alter cell proliferation and induce leukocyte infiltration, degeneration of luminal glandular epithelium, and hyperplasia in the various reproductive organs, and may also alter both embryonic and uterine IL-1a expression. IL-1a administration also caused implantation failure similar to that of LPS. The observations suggest that the determined MD of LPS may alter the expression of developmentally important proinflammatory cytokines such as IL-1a, which could, in turn, inhibit the normal processes of blastocyst implantation. Therefore, it is proposed that the LPS-induced histopathological alterations in the various reproductive organs of pregnant animals could be mediated by IL-1a and this may be one of the causes of failure of blastocyst implantation in the mouse.

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Endotoxin-induced and prostaglandin-mediated effects on corpus luteum function in the mare

Cited by 26 publications

References 10 publications

Quercetin and Bornyl Acetate Regulate T‐Lymphocyte Subsets and INF‐γ/IL‐4 Ratio In Utero in Pregnant Mice

Quercetin and Bornyl Acetate Regulate T‐Lymphocyte Subsets and INF‐γ/IL‐4 Ratio In Utero in Pregnant Mice

Effect of Salmonella Endotoxin Administered to the Pregnant Sheep at 133–142 Days Gestation on Fetal Oxygenation, Maternal and Fetal Adrenocorticotropic Hormone and Cortisol, and Maternal Plasma Tufnor Necrosis Factor α Concentrations1

A ‘minimum dose’ of lipopolysaccharide required for implantation failure: assessment of its effect on the maternal reproductive organs and interleukin-1α expression in the mouse

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