Prenatal stress alters immune function in the offspring of rats

Klein, Sabra L.; Rager, Dawn R.

doi:10.1002/dev.420280603

Cited by 74 publications

(36 citation statements)

References 54 publications

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“…Other studies showed only a decrease in the CD8ϩ subsets (26) or a gender difference in splenocyte response to mitogens, but no difference in the T-lymphocyte subsets (30). Prenatal stress is also associated with an altered response to stimulation with LPS (28) or the potent mitogen concanavalin A (27,29). The wide spectrum of results seen in these studies is likely a function of the model variance in type, onset, and duration of stress.…”

Section: Discussionmentioning

confidence: 73%

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Intrauterine Growth Restriction Alters T-Lymphocyte Cell Number and Dual Specificity Phosphatase 1 Levels in the Thymus of Newborn and Juvenile Rats

Contreras

Hale

et al. 2011

Pediatr Res

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Intrauterine growth restricted (IUGR) infants have increased susceptibility to infection associated with higher risk of illness and death. Dual specificity phosphatase 1 (DUSP1), which is transcribed in the thymus, increases in quantity as T cells mature and differentiate into CD4ϩ cells. Little is known about how IUGR affects DUSP1 levels and T-cell subpopulations over time. We hypothesized that IUGR would decrease cell count, CD4ϩ and CD8ϩ subpopulations of T lymphocytes, and DUSP1 levels in IUGR rat thymus and spleen. Bilateral uterine artery ligation produced IUGR rats. Thymus and spleen were harvested at P0 and P21. Flow cytometry was used to compare CD4ϩ and CD8ϩ lymphocyte populations. Real-time RT-PCR and Western blotting were used to determine DUSP1 quantity. IUGR significantly decreased total cell count in P0 and P21 IUGR male and female thymus. IUGR significantly increased CD4ϩ cells in IUGR P0 males and females, significantly decreased CD4ϩ cells in P21 female thymus, and significantly altered DUSP1 levels in the IUGR female thymus at P0 and P21, although it is not yet known whether the change in DUSP1 levels is due to a change in the level per cell or to a change in cellular composition of the thymus. (Pediatr Res 70: 123-129, 2011)

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Section: Discussionmentioning

confidence: 73%

“…These models include repeated stimulation of maternal rats to confrontation (25), acute immobilization (26), bright light (27,28), and loud noise (29,30). These studies have shown a decrease in total peripheral leukocyte count (26,31) and decreases in the peripheral CD4ϩ and CD8ϩ T-cell subsets in older rats (31).…”

Section: Discussionmentioning

confidence: 99%

Intrauterine Growth Restriction Alters T-Lymphocyte Cell Number and Dual Specificity Phosphatase 1 Levels in the Thymus of Newborn and Juvenile Rats

Contreras

Hale

et al. 2011

Pediatr Res

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“…Exposure of pregnant dams to footshock stress, psychological stress, and noise stress has all been shown to alter IgG levels in juvenile rats (19), and prenatal noise stress exposure has also been shown to reduce arthus skin reactions and delayed-type hypersensitivity reactions in offspring. Adult rat offspring of prenatally stressed dams also exhibit increased antibody response to antigen, although prenatal stress effects are less marked for natural killer (NK) cell cytotoxicity and are not observed for splenocyte proliferative responses to mitogens (20). These data are further confirmed by observations of Kay et al (21) that prenatal stress exposure reduces NK cell cytotoxicity in both the spleen and the blood but that these effects are less pronounced for splenocyte responses to phytohemagglutinin.…”

Section: Prenatal Maternal Influencesmentioning

confidence: 64%

The maternal-neonatal neuro-immune interface: Are there long-term implications for inflammatory or stress-related disease?

Shanks

Lightman²

2001

J. Clin. Invest.

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Inflammatory stimuli reliably elicit hypothalamic-pituitary-adrenal (HPA) activation, and it is now established that the immune and HPA systems are mutually regulatory and that their interactions partly determine stress effects on immune function. What has not been extensively investigated, however, is the interactive nature of the development of the endocrine and immune systems and whether this might alter predisposition to inflammatory disease or stress-related pathologies. Increasing attention is now being focused on the role of early life environments determining longterm predisposition to disease, and a role for the HPA axis in disease predisposition is emerging.Stress generally refers to the condition where coping with actual or perceived stimuli alters the homeostatic state of the organism. The classic stress response involves the activation of central and peripheral catecholamine systems and HPA responses. Increased glucocorticoid levels are thought to protect the organism, both by providing energy substrates to deal with immediate environmental demands and by blocking potentially harmful overreaction by the immune system and other stress-reactive systems (1). However, to avoid immunosuppression and degenerative pathologies associated with increased glucocorticoid levels, the HPA stress response must terminate efficiently once the environmental demands are removed (2). Consequently, disturbances in endocrine-immune interactions upset the normal regulatory homeostatic balance and alter susceptibility to a variety of disease states associated with immune dysregulation (3).The physiological impact of stress is variable across individuals, and susceptibility to stress apparently depends on attributes of the organism, such as genetic endowment and age, and experiential factors, such as previous stress experiences, and early life events (4, 5). Indeed, the endocrine and immune systems and the CNS all respond to environmental pressures during development, and the interactive nature of these systems suggests that alterations in one system could have developmental consequences for the others and potential long-term implications for disease vulnerability. Plasticity in most developing physiological systems is thought to be of adaptive importance, enabling an organism to better meet the demands of the environment in which it matures and will most likely reside. However, the short-term reorganization or re-setting of regulatory systems to deal with immediate demands may also have long-term consequences for normal physiological function, thereby predisposing an organism to pathology. This may particularly be the case when the environmental pressures differ between development and adulthood.A number of epidemiological studies have indicated that nutritional factors early in life have long-term implications for cardiovascular and metabolic disease in adulthood. Most data suggest that maternal nutrition and limited intrauterine growth are responsible for reorganizing metabolic regulation and results in metabolic and car...

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“…Previous research involving prenatal manipulation and immune function in the offspring has focused on the effects of environmental toxins, dietary alterations and various pharmaceuticals (Silva et al 1968, Roberts & Chapman 1981, Schmidt 1984. Daily handling, anxiety, electric foot-shocks, restraint with or without bright lights and elevated temperatures, noise, crowding and other stressor stimuli applied to dams can cause these changes in their adult offspring (Ader & Plaut 1968, Fride & Weinstock 1984, 1989, Harvey & Chevins 1985, Sobrian 1988, VonSaal et al 1991, Sobrian et al 1992, Klein & Rager 1995, Silva & Palermo-Neto 1999, Williams et al 1999a. In contrast, power frequency alternating magnetic fields had no effect on reproduction and prenatal development of mice (Yasuyuki et al 2002).…”

mentioning

confidence: 99%

Role of TNF-α in prenatal alterations in dams of mice under thermal stress

et al. 2006

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The possible involvement of cytokines such as tumour necrosis factor-a (TNF-a), interleukin-1b (IL-1b) and interferon-g (IFN-g) that are suspected of causing pregnancy loss and miscarriage has been investigated in dams of mice subjected to hyperthermia. Thermal stress was induced by exposing mice dams at 40721C for 4 h every day during the different phases of the gestation period whereas the normothermic animals were housed at 22721C. The effect of maternal thermal stress was measured in pregnant mice at different phases of the gestation period namely, blastogenesis-implantation phase (days 0-5 postconceptionem [p.c.]), organogenesis or embryogenesis phase (days 6-15 p.c.) and fetogenesis phase (days 16-20 p.c.). Uterine examination of dams subjected to hyperthermia on days 6-15 p.c. showed maximum reduction in live fetus number, gestational index and maximum pre-and postimplantation loss in comparison with dams housed in normothermic environment and dams exposed to thermal stress between days 0-5 and 16-20 p.c. Maximum resorption rate and number of non-viable fetuses were observed in dams exposed to hyperthermia during days 6-15 p.c. Elevated levels of TNF-a and IL-1b were observed in the amniotic fluid of dams subjected to hyperthermia during days 6-15 p.c. but IFN-g levels remained unaltered. Single intraperitoneal (i.p.) administration of recombinant mouse TNF-a at a dose of 1 and 0.5 ng/ mice in dams on day 6 in normothermic condition resulted in a reduced number of live fetuses. Administration of anti-TNF-a antibody i.p. at a dose of 10 mg/dam on day 6 p.c. and subjected to thermal stress between days 6-15 p.c. increased marginally the number of fetuses but failed to attain statistical significance in comparison with days 6-15 p.c. thermally stressed dams without antibody treatment. It is concluded that the induction of TNF-a, in the amniotic fluid is associated with thermal stress during pregnancy and may be linked to the reproductive performances of dams. This study will help in understanding the mechanism of thermal injury in pregnant subjects.

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Prenatal stress alters immune function in the offspring of rats

Cited by 74 publications

References 54 publications

Intrauterine Growth Restriction Alters T-Lymphocyte Cell Number and Dual Specificity Phosphatase 1 Levels in the Thymus of Newborn and Juvenile Rats

Intrauterine Growth Restriction Alters T-Lymphocyte Cell Number and Dual Specificity Phosphatase 1 Levels in the Thymus of Newborn and Juvenile Rats

The maternal-neonatal neuro-immune interface: Are there long-term implications for inflammatory or stress-related disease?

Role of TNF-α in prenatal alterations in dams of mice under thermal stress

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