Prenatal Endocrine Activation Alters Postnatal Cellular Immunity in Infant Monkeys

Coe, Christopher L.; Lubach, Gabriele R.; Karaszewski, Joseph W.; Ershler, William B.

doi:10.1006/brbi.1996.0020

Cited by 69 publications

(35 citation statements)

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“…With respect specifically to the monkey neonate, it extends to psychological stress our previous finding that endocrine activation of the mother affects the MLR of her newborn infant [12]. Further, the 2-day dexamethasone treatment commonly used in human obstetrical practice also impacted the neonate's MLR.…”

Section: Discussionmentioning

confidence: 85%

“…Our previous studies have demonstrated that acute activation of the gravid female's endocrine system by administration of adrenocorticotropic hormone or by psychological stressors can markedly affect the behavior and emotionality of the infants postnatally [9][10][11]. In addition, infant monkeys from pregnancies stimulated by adrenocorticotropic hormone for 2 weeks exhibited abnormal lymphocyte proliferative and cytolytic responses [12]. One alteration involved a failure of the neonate's cells to respond as readily when cultured in vitro with heterologous cells, either from the father or a genetically unrelated animal.…”

Section: Introductionmentioning

confidence: 99%

“…Our previous research compared the proliferative response of the neonate's cells to stimulator cells from the mother, father, and a genetically unrelated monkey [12]. The current assay also assessed responses to a virally transformed monkey cell line to test whether disturbance of the fetus at different points in development might alter the postnatal reaction to foreign antigenic proteins.…”

Section: Introductionmentioning

confidence: 99%

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Prenatal Stress and Immune Recognition of Self and Nonself in the Primate Neonate

Coe

Lubach

Karaszewski³

1999

Neonatology

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The capacity of the neonate to respond to nonself antigens was evaluated in infant monkeys born after normal and disturbed pregnancies. Mixed lymphocyte cultures were used to test the infants’ proliferative responses to mitomycin-treated stimulator cells, either from a genetically unrelated animal or from a virally transformed monkey cell line. Periods of daily stress for 6 weeks in mid-late pregnancy (months 3.0–4.5) resulted in a significant decrease in proliferative responses, whereas the same stressor early in pregnancy (months 1.5–3.0) increased responses by the neonate’s cells. Similar to the late stress effect, an inhibition of proliferative responses by neonatal cells was induced by dexamethasone administered for 2 days late in pregnancy at 4.5 months after conception, 1 month before term. These findings demonstrate that certain immune responses at birth are extremely sensitive to prior prenatal events. Further, the bidirectional changes indicate that there may be critical periods in gestation when the same extrinsic events have radically different effects on the fetus.

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Section: Discussionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Prenatal Stress and Immune Recognition of Self and Nonself in the Primate Neonate

Coe

Lubach

Karaszewski³

1999

Neonatology

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“…Perinatal stress and long-term changes to the HPA axis Numerous animal models have demonstrated associations between prenatal stress and long-term alterations in HPA axis function (Coe et al, 1996(Coe et al, , 1999Kapoor et al, 2006;Weinstock, 2005). Healthy young adult humans who had been exposed to prenatal stress, because their mothers had experienced severe negative life events during pregnancy, responded differently to a standardized social stressor (TSST) when compared to an age-matched comparison group of healthy young adults who had not been exposed to prenatal stress.…”

Section: 2mentioning

confidence: 99%

Hygiene and Other Early Childhood Influences on the Subsequent Function of the Immune System

Rook

2012

Immunity to Parasitic Infection

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Hygiene Depression a b s t r a c tThe immune system influences brain development and function. Hygiene and other early childhood influences impact the subsequent function of the immune system during adulthood, with consequences for vulnerability to neurodevelopmental and psychiatric disorders. Inflammatory events during pregnancy can act directly to cause developmental problems in the central nervous system (CNS) that have been implicated in schizophrenia and autism. The immune system also acts indirectly by "farming" the intestinal microbiota, which then influences brain development and function via the multiple pathways that constitute the gut-brain axis. The gut microbiota also regulates the immune system.Regulation of the immune system is crucial because inflammatory states in pregnancy need to be limited, and throughout life inflammation needs to be terminated completely when not required; for example, persistently raised levels of background inflammation during adulthood (in the presence or absence of a clinically apparent inflammatory stimulus) correlate with an increased risk of depression. A number of factors in the perinatal period, notably immigration from rural low-income to rich developed settings, caesarean delivery, breastfeeding and antibiotic abuse have profound effects on the microbiota and on immunoregulation during early life that persist into adulthood. Many aspects of the modern western environment deprive the infant of the immunoregulatory organisms with which humans co-evolved, while encouraging exposure to nonimmunoregulatory organisms, associated with more recently evolved "crowd" infections.

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“…In fact, exposure of animals to stress during critical periods of development have long-lasting effects, among others on physical development, neurochemical and behavioral parameters, regulation of the hypothalamic-pituitary-adrenal (HPA) axis and immunocompetence of the offspring [9, 28, 35,37,38,39]. The effects of prenatal stress vary considerably depending on the nature, intensity and duration of the stressor, as well as on the stage of gestation at the time of stressor application [2, 7]. In rats and mice, maternal stress-induced alterations are more frequently reported when the stressor is applied during the last third of pregnancy, a period including differentiation on the gonads, the reproductive tract, lymphoid organs and brain [17, 38].…”

Section: Introductionmentioning

confidence: 99%

Naloxone Treatment Prevents Prenatal Stress Effects on Peritoneal Macrophage Activity in Mice Offspring

Fonseca

Sakai²,

Carvalho-Freitas³

et al. 2005

Neuroendocrinology

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The present study analyzed the effects of maternal stress (PS) and/or naloxone treatment on the activity of peritoneal macrophage in male and female Swiss mice offspring. Pregnant female rats received a daily footshock (0.2 mA) and/or a naloxone injection from gestational day 15 to 19. Experiments were performed on postnatal day 30 on male and female pups. The following results were obtained in male offspring: (1) PS decreased both the index and the percentage of phagocytosis, this decrement being reversed by naloxone treatment, and (2) naloxone alone decreased the percentage of phagocytosis. The following results were obtained in female offspring: (1) PS decreased spontaneous and phorbol myristate acetate-induced macrophage oxidative burst, this decrement being reversed by naloxone pretreatment, and (2) PS decreased both the index and percentage of the phagocytosis, this effect was prevented by naloxone treatment. These data are discussed focussing on a putative neuroimmune interaction involving opioidergic systems during the ontogeny of the central nervous and immune systems.

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Prenatal Endocrine Activation Alters Postnatal Cellular Immunity in Infant Monkeys

Cited by 69 publications

References 0 publications

Prenatal Stress and Immune Recognition of Self and Nonself in the Primate Neonate

Prenatal Stress and Immune Recognition of Self and Nonself in the Primate Neonate

Hygiene and Other Early Childhood Influences on the Subsequent Function of the Immune System

Naloxone Treatment Prevents Prenatal Stress Effects on Peritoneal Macrophage Activity in Mice Offspring

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