Nonspecific Immunopotentiators and Pregnancy Loss: Complete Freund Adjuvant Reverses High Fetal Resorption Rate in CBA × DBA/2 Mouse Combination

Toder, V.; Strassburger, D.; Irlin, Y.; Carp, Howard; Pecht, M; Trainin, Nathan

doi:10.1111/j.1600-0897.1990.tb01040.x

Cited by 39 publications

(11 citation statements)

References 20 publications

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“…It was earlier demonstrated that maternal immunopotentiation may increase the embryo's resistance to the effect of the embryolethal and teratogenic stimuli, whether chemical, physical, or intrinsic [21,[30][31][32]. In this work, we have found that maternal immunopotentiation increased the level of TGF-β2 mRNA and protein expression in the uteri and placentae of diabetic mice at all examined time points.…”

Section: Discussionsupporting

confidence: 63%

Diabetes teratogenicity in mice is accompanied with distorted expression of TGF‐β2 in the uterus

Fein

Magid

Savion

et al. 2001

Teratog Carcinog Mutagen

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Early embryonic deaths as well as malformed newborns are among complications of the diabetic pregnancy. Cytokines and growth factors operating in the embryonic vicinity are found to be among factors that determine the sensitivity of embryos to external and internal detrimental stimuli, including diabetes. Transforming Growth Factor-β2 (TGF-β2) has been shown to be essential for embryonic development and survival. In the present work, we evaluated the pattern of TGF-β2 expression in the uterus of streptozotocin-induced diabetic mice, demonstrating a decreased reproductive performance and elevated percentage of litters with severely malformed fetuses. Since stimulation of the maternal immune system was found to increase the resistance of mouse embryos to the teratogenic effect of diabetes, the effect of immunopotentiation on the expression of the cytokine was also investigated. TGF-β2 expression was studied at the mRNA level by using the in situ hybridization technique and at the protein level by using the immunohistochemical analysis. A clear decrease in TGF-β2 mRNA expression in the uterus of diabetic mice was observed at examined time points: days 1, 5, and 9 of pregnancy. Also, an evident reduction in TGF-β2, the protein expression in the uterus of diabetic mice, was demonstrated at these time points. Maternal immunopotentiation that improved the reproductive performance of diabetic mice and reduced the number of the litters with malformed fetuses was also accompanied by a clear increase in the level of TGF-β2 mRNA expression in the pregnant uteri. The above results clearly demonstrate that the embryotoxic effect of diabetes is accompanied by an alteration of TGF-β2 ex- pression. Immunopotentiation that was shown to improve the reproductive performance of the diabetic mice was accompanied by a partial normalization of TGF-β2 expression in embryonic vicinity. Teratogenesis Carcinog. Mutagen. 22:59-71, 2002.

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Section: Discussionsupporting

confidence: 63%

Diabetes teratogenicity in mice is accompanied with distorted expression of TGF‐β2 in the uterus

Fein

Magid

Savion

et al. 2001

Teratog Carcinog Mutagen

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“…1,12 -14 Also, nonspecific immunomodulation with CFA was shown by us to decrease fetal loss in the CBA/JxDBA/2J model, an effect that was associated with an increased number of Mac-1-positive cells in the spleen and placenta and an increased production of IL-1. 15,3 In parallel, it was shown in several mouse models of pregnancy loss that various cytokines are capable of controlling fetal survival by decreasing the resorption rate and supporting placental growth and function. [16][17][18] This data concer with the well established role of various cytokines (especially CSFs), in supporting placental growth and fetal survival.…”

Section: Discussionmentioning

confidence: 99%

Ciprofloxacin Affects Pregnancy Loss in CBA/JxDBA/2J Mice Possibly via Elevation of Interleukin‐3 and Granulocyte Macrophage‐Colony Stimulating Factor Production

Savion¹,

Blank²,

Shepshelovich³

et al. 2000

American J Rep Immunol

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“…Also, non-speci®c immunopotentiation with Freund's complete adjuvant (FCA) or xenogeneic lymphocytes may improve the reproductive performance of mice with spontaneous pregnancy loss [28,31,34,37]. Although the precise mechanisms whereby immunostimulation prevents embryo loss are still unknown, it has been suggested that immunostimulation may result in modulation of the cytokine milieu in the embryonic microenvironment, leading to enhanced production of Th2 cytokines and suppression of Th1-type immune responses [38,39].…”

Section: Discussionmentioning

confidence: 99%

Colony-stimulating factor-1 (CSF-1) expression in the uteroplacental unit of mice with spontaneous and induced pregnancy loss

Gorivodsky

Torchinsky

Shepshelovich

et al. 1999

Clinical and Experimental Immunology

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CSF-1 plays an important role in female reproduction and normal embryo development. To understand further CSF-1 function in normal and, especially, in compromised pregnancy, we studied the pattern of its mRNA expression as well as expression of its receptor (c-fms) in the uteroplacental units of mice with induced (cyclophosphamide (CY)-treated) and spontaneous (CBA/J x DBA/2J mating combination) pregnancy loss. RNase protection analysis demonstrated the presence of two forms of CSF-1 mRNA in the uteroplacental unit corresponding to 1400- and 263-bp protective fragments. Densitometric analysis demonstrated that the level of 1400-bp mRNA form was decreased by 40% in the uteroplacental units of mice with CY-induced pregnancy loss compared with the control mice. About 20% decrease in 263-bp protective fragment was registered in resorbing versus non-resorbed placenta of CBA/J females mated to DBA/2J males. As judged by in situ hybridization assay, CSF-1 mRNA transcripts were localized in the uterine epithelium and stroma, while c-fms mRNA was found mainly in the trophoblast. The number of metrial gland cells as well as the number of uterine leucocytes expressing CSF-1 and c-fms mRNAs was substantially lower in the uteroplacental unit of mice with pregnancy loss than in control animals. Maternal immunostimulation, while significantly decreasing the resorption rate in mice with CY-induced pregnancy loss, also strengthened CSF-1 mRNA expression at the fetomaternal interface and resulted in reconstitution in the number of CSF-1+ uterine leucocytes and metrial gland cells. These data suggest a role for uterine CSF-1 in the physiology of normal and compromised pregnancy and demonstrate a possible involvement of CSF-1-associated signalling in mechanisms of placenta and endometrium repair following immunopotentiation.

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Nonspecific Immunopotentiators and Pregnancy Loss: Complete Freund Adjuvant Reverses High Fetal Resorption Rate in CBA × DBA/2 Mouse Combination

Cited by 39 publications

References 20 publications

Diabetes teratogenicity in mice is accompanied with distorted expression of TGF‐β2 in the uterus

Diabetes teratogenicity in mice is accompanied with distorted expression of TGF‐β2 in the uterus

Ciprofloxacin Affects Pregnancy Loss in CBA/JxDBA/2J Mice Possibly via Elevation of Interleukin‐3 and Granulocyte Macrophage‐Colony Stimulating Factor Production

Colony-stimulating factor-1 (CSF-1) expression in the uteroplacental unit of mice with spontaneous and induced pregnancy loss

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