Elevated Circulating IL-1<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>β</mml:mi></mml:math>and TNF-Alpha, and Unaltered IL-6 in First-Trimester Pregnancies Complicated by Threatened Abortion With an Adverse Outcome

Vitoratos, N.; Papadias, C.; Economou, Emmanuel; Makrakis, Evangelos; Panoulis, Constantinos; Creatsas, George

doi:10.1155/mi/2006/30485

Cited by 41 publications

(29 citation statements)

References 22 publications

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“…12 However, few have come across elevated circulating IL-1B and TNF-α and unaltered IL-6 in first trimester pregnancies complicated by threatened miscarriage with an adverse pregnancy outcome. 13 They concluded that this distinct immune response was relevant to predict negative outcome of pregnancy. In our study, we found significantly higher levels of IL-2 and lower values of IL-6 in threatened aborters who aborted in comparison to control.…”

Section: Discussionmentioning

confidence: 99%

Study of TH 1 and TH 2 activity in women with threatened miscarriages

Jain

Hassan

Jain

2015

Int J Reprod Contracept Obstet Gynecol

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Section: Discussionmentioning

confidence: 99%

Study of TH 1 and TH 2 activity in women with threatened miscarriages

Jain

Hassan

Jain

2015

Int J Reprod Contracept Obstet Gynecol

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“…However, fine tuning is the backbone of neonatal innate immunity. The fetus calls for the prevention of any proinflammatory immune response [16,30,31] , whereas the newborn needs a competent and efficient immune response because it is no longer mechanically hooded or even protected by the mother's immune system [16] . mi-RNA-146 might represent a crucial element in the regulation of these antipodal demands.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-146: Tiny Player in Neonatal Innate Immunity?

Lederhuber

Bær²,

Altiok³

et al. 2010

Neonatology

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Background: Concise regulation of the Toll signaling pathway is mandatory in neonatal innate immunity. The microRNA-146 family (miR-146a/b) was recently reported to be a regulator of Toll-like receptor 4 (TLR4) through a negative feedback loop mechanism. Acting as a potent regulator, miRNA helps to protect the organism from developing overwhelming proinflammatory immune responses leading to septic shock or chronic inflammatory diseases. Objective: We investigated for the first time whether miRNA-146a/b plays a regulatory role in human monocytes derived from infant cord or adult blood, and whether differences in miRNA-146 expression exist. Methods: Expression profiles of miR-146a/b and TLR4 were studied by real-time PCR upon stimulation with lipopolysaccharide. Results: Both members of the miRNA-146 family showed a time-dependent upregulation. For miR-146a, a statistically higher significant increase was found after 24 h of stimulation in monocytes from cord blood compared to those derived from adults. In contrast, no differences were found for miR-146b and TLR4, respectively. Conclusion: We conclude that differences between the negative regulatory role for miR-146a obviously exist in neonatal and adult TLR4 signaling, and suggest that more intense research in the involvement of miRNA in immune regulation will facilitate the understanding of the development and function of the innate immune system of neonates.

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“…Elevated TNF-α levels in maternal serum in the first-trimester in threatened abortion patients correlates with a poor outcome. In contrast, TNF-α levels are lower in uncomplicated pregnancy and threatened abortion patients with a good outcome, indicating that elevated TNF-α levels may be related to an adverse obstetric outcome in patients with threatened abortion [25]. shallow invasion of trophoblasts to decidua has been implicated in poor pregnancy outcome including IUGR and PIH [2,3].…”

Section: Discussionmentioning

confidence: 99%

Tumor Necrosis Factor-.ALPHA. (TNF-.ALPHA.) Inhibits Insulin-like Growth Factor-I (IGF-I) Activities in Human Trophoblast Cell Cultures Through IGF-I/Insulin Hybrid Receptors

et al. 2010

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TrophoblasT cells invade to the decidual tissue, and remodel uterine spiral arteries in human early placenta [1]. Appropriate trophoblasts migration is critical for fetal and placental development, and shallow invasion of trophoblast cells has been involved in intrauterine growth restriction (IUGR) and pregnancyinduced hypertension (PIH) [2,3]. Many endocrine factors and cytokines have been involved in placental development, including tumor necrosis factor-α (TNF-α) and insulin-like growth factors (IGFs).Tumor necrosis factor-α (TNF-α) is a cytotoxic molecule produced predominantly by macrophages abstract. Tumor necrosis factor-α (TNF-α) in placenta is believed to be involved in pathogenesis of intrauterine growth restriction. In contrast, insulin-like growth factors (IGFs) are believed to be important for stimulation of fetal and placental growth. IGF-I stimulates metabolic and growth-promoting actions directly through its receptors: IGF-I receptor (IGF-IR), insulin receptor (IR) and IGF-I/insulin hybrid receptor (HR). However, it has not been elucidated which receptor mediates the growth promoting effects in fetal and placental growth. The current studies were undertaken to test whether TNF-α affects IGF-I action on placenta using human trophoblast cell cultures, and to test which receptor mediates growth promoting effects of IGF-I in placenta. Primary culture of trophoblast cells, which express IGF-IR, IR, and HR, were exposed to TNF-α, and the effects of IGF-I in stimulating trophoblast cell proliferation and migration were determined. exposure to TNF-α attenuated the effects of IGF-I on cell proliferation and migration. To determine which receptors are involved in this inhibitory effect, the ability of IGF-I to stimulate phosphorylation of its receptors was analyzed in the presence of TNF-α. TNF-α exposure neither attenuated the phosphorylation of IGF-IR homodimer by IGF-I nor changed receptor abundance. In contrast, TNF-α reduced the ability of IGF-I to stimulate phosphorylation of HR with reducing amounts of HR. exposure to TNF-α also attenuated phosphorylation of insulin receptor substrate-1 (IRs-1) and the association of IRS-1 with phosphatydilinositol-3 kinase (PI-3 kinase). Taken together, these findings indicate that TNF-α induces a loss of sensitivity to stimulation by IGF-I, through reducing amounts of HR and the stimulation of HR tyrosine kinase activity by IGF-I.

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Elevated Circulating IL-1βand TNF-Alpha, and Unaltered IL-6 in First-Trimester Pregnancies Complicated by Threatened Abortion With an Adverse Outcome

Cited by 41 publications

References 22 publications

Study of TH 1 and TH 2 activity in women with threatened miscarriages

Study of TH 1 and TH 2 activity in women with threatened miscarriages

MicroRNA-146: Tiny Player in Neonatal Innate Immunity?

Tumor Necrosis Factor-.ALPHA. (TNF-.ALPHA.) Inhibits Insulin-like Growth Factor-I (IGF-I) Activities in Human Trophoblast Cell Cultures Through IGF-I/Insulin Hybrid Receptors

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