Diabetes teratogenicity is accompanied by alterations in macrophages and T cell subpopulations in the uterus and lymphoid organs

Savion, Shoshana; Gidon-Dabush, S; Fein, Amos; Torchinsky, Arkady; Toder, V.

doi:10.1016/j.intimp.2004.05.018

Cited by 6 publications

(3 citation statements)

References 26 publications

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“…However, there have been few studies on effects of diabetes on endometrial leukocytes [22]. The present study reports that pregnancy significantly increased NK, macrophage and total leucocyte population in the endometrium.…”

Section: Discussionmentioning

confidence: 44%

Immunohistochemical investigation of endometrial leukocytes in implantation period in rats with streptozotosin-induced diabetes

Nacar

Bozkurt²,

Köç³

et al. 2016

pjp

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Our first aim was to determine the total leukocyte profile in implantation. Second aim was to detect the changes in uterine leukocyte profile in diabetes, a common accompanying disease. For this purpose 4 groups are formed with Wistar albino rats weighing 250-300 g. Two of the groups were non-diabetic and two of them were diabetic. One of the diabetic and one of the non-diabetic groups were left pregnant. Then uterus tissues of pregnant animals were removed in the 5 th and 7 th days of pregnancy together with tissues of other two non-pregnant groups. Tissues were analyzed immunohistochemically with antibodies CD45, CD3, CD4, CD8, CD56, CD68 and CD79a. It was revealed that pregnancy increased immune staining of CD68, CD3, CD45 and CD56 in endometrium. In addition it was observed that immune staining density of CD68, CD45 and CD56 decreased in diabetes.In the histopathological examination, significant degeneration was detected in the endometrium of diabetic rats. Diabetes could decrease leukocyte proportions in decidua in early pregnancy periods. Therefore immune cell therapies could be administrated in diabetes related problems of pregnancy.

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Section: Discussionmentioning

confidence: 44%

Immunohistochemical investigation of endometrial leukocytes in implantation period in rats with streptozotosin-induced diabetes

Nacar

Bozkurt²,

Köç³

et al. 2016

pjp

View full text Add to dashboard Cite

show abstract

“…A higher risk of congenital malfor-mations has been assessed in diabetic pregnancy than in normal, non-diabetic pregnancy (Eriksson, 2009). This teratogenicity might be partly related to macrophages localized to the uterus and the lymphoid organs as derived from results from a streptozotocininduced diabetes model in ICR mice (Savion et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Modulation of macrophage inflammatory profile in pregnant nonobese diabetic (NOD) mice

Larocca

Hauk

Calafat

et al. 2011

Molecular and Cellular Endocrinology

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“…Diverse means of stimulating the maternal immune system, such as intraperitoneal (IP) injection of inert particles, intrauterine injection of xenogenic lymphocytes or intrauterine or IP injection of immunostimulatory cytokines, have been effective in preventing or reducing fetal defects (Hrubec et al, 2005). The specific operating mechanisms responsible for the reduction in fetal dysmorphogenesis are unknown; however, the collective literature suggests that immunoregulatory cytokines of maternal origin may normalize dysregulated apoptosis and or cell proliferation in the fetus (Sharova et al, 2000; Punareewattana and Holladay, 2004; Savion et al, 2004). …”

Section: Introductionmentioning

confidence: 99%

Modulation of Diabetes‐Induced Palate Defects by Maternal Immune Stimulation

Hrubec

Toops

Holladay

2008

The Anatomical Record

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Maternal diabetes can induce a number of developmental abnormalities in both laboratory animals and humans, including deformities of the face and palate. The incidence of birth defects in newborns of women with diabetes is approximately 3 to 5 times higher than among nondiabetics. In mice, nonspecific activation of the maternal immune system can reduce fetal abnormalities caused by various etiologies including hyperglycemia. This study was conducted to determine whether nonspecific maternal immune stimulation could reduce diabetes-induced palate defects and orofacial clefts. Female ICR mice were immune stimulated before induction of hyperglycemia with Freund's complete adjuvant (FCA), granulocyte-macrophage colony-stimulating factor (GM-CSF), or interferon-g (IFNg). Streptozocin was used to induce hyperglycemia (26-35 mmol blood glucose) in females before breeding. Fetuses from 12 to 18 litters per treatment group were collected on Day 17 of gestation. Palate width and length were measured, and the incidence of orofacial clefts was determined. Palate length and width were both decreased by maternal hyperglycemia. Maternal immune stimulation with GM-CSF or FCA limited the degree of palate shortening from the hyperglycemia. Each of the three immune stimulants attenuated significant narrowing of the palate. Rates of orofacial clefts were not significantly different between treatment groups. Palatogenesis is a complex process driven by cellular signals, which regulate cell growth and apoptosis. Dysregulation of cellular signals by maternal hyperglycemia can result in fetal malformations. Maternal immune stimulation may prevent dysregulation of these signaling pathways thus reducing fetal malformations and normalizing palate growth.

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Diabetes teratogenicity is accompanied by alterations in macrophages and T cell subpopulations in the uterus and lymphoid organs

Cited by 6 publications

References 26 publications

Immunohistochemical investigation of endometrial leukocytes in implantation period in rats with streptozotosin-induced diabetes

Immunohistochemical investigation of endometrial leukocytes in implantation period in rats with streptozotosin-induced diabetes

Modulation of macrophage inflammatory profile in pregnant nonobese diabetic (NOD) mice

Modulation of Diabetes‐Induced Palate Defects by Maternal Immune Stimulation

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