Antenatal endogenous and exogenous glucocorticoids and their impact on immune ontogeny and long-term immunity

Solano, María Emilia; Holmes, Megan C.; Mittelstadt, Paul R.; Chapman, Karen

doi:10.1007/s00281-016-0575-z

Cited by 45 publications

(62 citation statements)

References 273 publications

(381 reference statements)

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“…Glucocorticoids can affect placental gene expression and growth (6,125), with consequences in the nutrition and gas exchange with the fetus. These effects together with potential fetal excessive glucocorticoid exposure are hypothesized to underlie intrauterine growth restriction i.e., in the case of maternal dietary protein restriction, or stress [reviewed in (8)].…”

Section: Intrauterine Growth Restrictionmentioning

confidence: 99%

“…During late gestation, glucocorticoids are required to ensure structural and functional organ maturation in the fetus (126,127). However, prenatal exposure to glucocorticoid surges is detrimental for fetal growth and may hold significant consequences for postnatal physiology (8). Fetal glucocorticoid excess can be induced e.g., by antenatal steroid treatments in the case of risk for preterm birth (128).…”

Section: Prenatal Exposure To Excess Glucocorticoids: Fetal Programmimentioning

confidence: 99%

“…Growing evidence underscores a role of prenatal glucocorticoid exposure in offspring's immune ontogeny and impaired postnatal immunity (131,132). These effects could be multifactorial, including indirect and direct effects in the immune system (8). For instance, prenatal stress or glucocorticoid excess can result in disarrangements in the HPA [reviewed e.g., in (133)].…”

Section: Prenatal Exposure To Excess Glucocorticoids: Fetal Programmimentioning

confidence: 99%

“…Both postnatal HPA and metabolism may affect postnatal immune responses. Remarkably, premature exposure to glucocorticoids may also affect the developing fetal immune system [reviewed in (8)]. For example, antenatal steroid treatment resulted in newborns with impaired immunity (136) e.g., due to poor neutrophil (137) and T cell (138) responses.…”

Section: Prenatal Exposure To Excess Glucocorticoids: Fetal Programmimentioning

confidence: 99%

“…Additionally to sex steroids, maternal glucocorticoids dramatically increase over the course of pregnancy in order to meet the increasing energy demands (6). Glucocorticoids are potent activators of GR, and this activation has pleiotropic effects on immune cells (7,8). However, the molecular mechanisms underlying how glucocorticoids contribute to the maternal immune adaptation to pregnancy and the interplay between glucocorticoids and sex hormones such as progesterone remain largely unclear.…”

Section: Introductionmentioning

confidence: 99%

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Steroids, Pregnancy and Fetal Development

2020

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Maternal glucocorticoids critically rise during pregnancy reaching up to a 20-fold increase of mid-pregnancy concentrations. Concurrently, another steroid hormone, progesterone, increases. Progesterone, which shows structural similarities to glucocorticoids, can bind the intracellular glucocorticoid receptor, although with lower affinity. Progesterone is essential for the establishment and continuation of pregnancy and it is generally acknowledged to promote maternal immune tolerance to fetal alloantigens through a wealth of immunomodulatory mechanisms. Despite the potent immunomodulatory capacity of glucocorticoids, little is known about their role during pregnancy. Here we aim to compare general aspects of glucocorticoids and progesterone during pregnancy, including shared common steroidogenic pathways, plasma transporters, regulatory pathways, expression of receptors, and mechanisms of action in immune cells. It was recently acknowledged that progesterone receptors are not ubiquitously expressed on immune cells and that pivotal features of progesterone induced-maternal immune adaptations to pregnancy are mediated via the glucocorticoid receptor, including e.g., T regulatory cells expansion. We hypothesize that a tight equilibrium between progesterone and glucocorticoids is critically required and recapitulate evidence supporting that their disequilibrium underlie pregnancy complications. Such a disequilibrium can occur, e.g., after maternal stress perception, which triggers the release of glucocorticoids and impair progesterone secretion, resulting in intrauterine inflammation. These endocrine misbalance might be interconnected, as increase in glucocorticoid synthesis, e.g., upon stress, may occur in detriment of progesterone steroidogenesis, by depleting the common precursor pregnenolone. Abundant literature supports that progesterone deficiency underlies pregnancy complications in which immune tolerance is challenged. In these settings, it is largely yet undefined if and how glucocorticoids are affected. However, although progesterone immunomodulation during pregnancy appear to be chiefly mediated glucocorticoid receptors, excess glucocorticoids cannot compensate by progesterone deficiency, indicating that additional und still undercover mechanisms are at play.

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Section: Intrauterine Growth Restrictionmentioning

confidence: 99%

Section: Prenatal Exposure To Excess Glucocorticoids: Fetal Programmimentioning

confidence: 99%

Section: Prenatal Exposure To Excess Glucocorticoids: Fetal Programmimentioning

confidence: 99%

Section: Prenatal Exposure To Excess Glucocorticoids: Fetal Programmimentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Steroids, Pregnancy and Fetal Development

2020

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Expansion of human γδ T cells in periphery: Lessons learned from development, infections, and compromised thymic function

Ravens,

Tolosa

2024

Eur J Immunol

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Abstractγδ T cells predominantly develop in the fetal period. Post birth they respond swiftly to environmental insults, pathogens and tumors, especially when other immune effector cells are less ready to function. Most of our understanding of γδ T‐cell development, peripheral adaptation, and function derives from murine studies. The recent advancement of immunological methods allows now to decipher human γδ T‐cell biology in patient cohorts and tissue samples, and to manipulate them using in vitro systems. In this review, we summarize γδ T‐cell development in the human thymus, their functional adaptation to the microbial environment from birth until old age, and their capacity to expand and fill up the peripheral niche under conditions of perturbations of conventional T‐cell development.

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Maternal psychiatric status and infant wheezing: The role of maternal hormones and cord blood cytokines

Yılmaz

Yaşar

Polat

et al. 2021

Pediatric Pulmonology

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Rationale: Maternal psychosocial stress might be associated with development of allergic diseases in the offspring.Objectives: To evaluate the association of maternal depression and anxiety with ever wheezing and recurrent wheezing among infants and to assess the role of maternal hypothalamo-pituatary-adrenal axis changes and fetal immune response in this association.Methods: This study encompasses two designs; cohort design was developed to evaluate the association of prenatal depression with development of wheezing in infants while nested case-control design was used to assess the role of maternal cortisol and tetranectin and cord blood interleukin 13 and interferon γ.Results: We enrolled 697 pregnant women. Elementary school graduate mother (odds ratio [OR] = 1.5, p = .06), maternal smoking during pregnancy (OR = 3.4, p = .001), familial history of asthma (OR = 2.7, p < .001) increased the risk of ever wheezing. Elementary school graduate mother (OR = 2.6, p = .002), maternal smoking during pregnancy (OR = 4.8, p < .001) and familial history of asthma (OR = 1.7, p = .01) increased the risk of recurrent wheezing. Maternal previous psychiatric disease, or Edinburgh Postnatal Depression Scale or Spielberger State-Trait Anxiety Inventory scores were not associated with wheezing. Maternal tetranectin levels were significantly higher among never wheezers compared to the ever wheezers (264.3 ± 274.8 vs. 201.6 ± 299.7, p = .04). Conclusions:In conclusion, the major risk factors for ever wheezing and recurrent wheezing were maternal smoking, level of education and family history of asthma. However, maternal depression and anxiety were not determined as risk factors for wheezing. Maternal tetranectin carries potential as a biomarker for wheezing in the infant.

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Antenatal endogenous and exogenous glucocorticoids and their impact on immune ontogeny and long-term immunity

Cited by 45 publications

References 273 publications

Steroids, Pregnancy and Fetal Development

Steroids, Pregnancy and Fetal Development

Expansion of human γδ T cells in periphery: Lessons learned from development, infections, and compromised thymic function

Maternal psychiatric status and infant wheezing: The role of maternal hormones and cord blood cytokines

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