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Dataset describing maternal prenatal restraint stress effects on immune factors in mice.

ABSTRACT: Maternal immune dysregulation, caused by gestational psychological stress, infection, and other perturbations, results in altered offspring neurodevelopment and increases risk for psychiatric disorders. Prior work has found that multiple cytokines play critical roles in shaping offspring neurodevelopment after gestational stress, though how maternal psychological stress impacts maternal, placental, and fetal cytokine levels more broadly remains unclear. The purpose of the present study was to assess changes to IL-1β, IL-2, IL-4, IL-6, IL-10, IL-17A, IFNγ, and TNFα in a widely-used mouse prenatal restraint stress model. After repetitive restraint stress on gestational days 12-14, stressed dams had increased serum levels of IL-1β, IL-6, and IL-10. Embryonic day 14 IL-2 and IL-1β levels were decreased in prenatally stressed male fetal forebrain, while placental IL-2 was decreased by stress regardless of offspring sex. Placental and fetal forebrain IL-2 levels were negatively correlated. These data provide important insights into the immune changes that occur with prenatal restraint stress.

SUBMITTER: Gumusoglu SB

PROVIDER: S-EPMC9189994 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature

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Dataset describing maternal prenatal restraint stress effects on immune factors in mice.

Gumusoglu Serena Banu SB Maurer Sara Victoria SV Stevens Hanna Elizabeth HE

Data in brief 20220603

Maternal immune dysregulation, caused by gestational psychological stress, infection, and other perturbations, results in altered offspring neurodevelopment and increases risk for psychiatric disorders. Prior work has found that multiple cytokines play critical roles in shaping offspring neurodevelopment after gestational stress, though how maternal psychological stress impacts maternal, placental, and fetal cytokine levels more broadly remains unclear. The purpose of the present study was to as ...[more]

PMID: 35707242

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Project description:The developing immune system and central nervous system in the fetus and child are extremely sensitive to both exogenous and endogenous signals. Early immune system programming, leading to changes that can persist over the life course, has been suggested, and other evidence suggests that immune dysregulation in the early developing brain may play a role in neurodevelopmental disorders such as autism spectrum disorder and schizophrenia. The timing of immune dysregulation with respect to gestational age and neurologic development of the fetus may shape the elicited response. This creates a possible sensitive window of programming or vulnerability. This review will explore the effects of maternal prenatal and infant nutritional status (from conception until early childhood) as well as maternal prenatal stress and anxiety on early programming of immune function, and how this might influence neurodevelopment. We will describe fetal immune system development and maternal-fetal immune interactions to provide a better context for understanding the influence of nutrition and stress on the immune system. Finally, we will discuss the implications for prevention of neurodevelopmental disorders, with a focus on nutrition. Although certain micronutrient supplements have shown to both reduce the risk of neurodevelopmental disorders and enhance fetal immune development, we do not know whether their impact on immune development contributes to the preventive effect on neurodevelopmental disorders. Future studies are needed to elucidate this relationship, which may contribute to a better understanding of preventative mechanisms. Integrating studies of neurodevelopmental disorders and prenatal exposures with the simultaneous evaluation of neural and immune systems will shed light on mechanisms that underlie individual vulnerability or resilience to neurodevelopmental disorders and ultimately contribute to the development of primary preventions and early interventions.

Project description:Carnosine (?-alanyl-L-histidine), a naturally occurring dipeptide, has been characterized as a putative neurotransmitter and serves as a reservoir for brain histamine, which could act on histaminergic neurons system to relieve stress-induced damages. However, understanding of the role of carnosine in stress-evoked immunocompromise is limited. In this study, results showed that when mice were subjected to restraint stress, spleen index and the number of spleen lymphocytes including Natural Killer (NK) cells were obviously decreased. Results also demonstrated that restraint stress decreased the cytotoxic activity of NK cells per spleen (LU(10)/spleen) while the activity of a single NK cell (LU(10)/10(6) cells) was not changed. However, oral administration of carnosine (150 and 300 mg/kg) increased spleen index and number of spleen lymphocytes (including NK cells), and elevated the cytotoxic activity of NK cells per spleen in restraint-stressed mice. These results indicated that carnosine ameliorated stress-evoked immunocompromise through spleen lymphocyte number maintenance. Carnosine was further found to reduce stress-induced elevation of plasma corticosterone level. On the other hand, results showed that carnosine and RU486 (a glucocorticoids receptor antagonist) treatment prevented the reduction in mitochondrion membrane potential and the release of mitochondrial cytochrome c into cytoplasm, increased Bcl-2/Bax mRNA ratio, as well as decreased terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells in spleen lymphocytes of stressed mice. The results above suggested that the maintenance of spleen lymphocyte number by carnosine was related with the inhibition of lymphocytes apoptosis caused by glucocorticoids overflow. The stimulation of lymphocyte proliferation by carnosine also contributed to the maintenance of spleen lymphocyte number in stressed mice. In view of the elevated histamine level, the anti-stress effects of carnosine on restraint-evoked immunocompromise might be via carnosine-histamine metabolic pathway. Taken together, carnosine maintained spleen lymphocyte number by inhibiting lymphocyte apoptosis and stimulating lymphocyte proliferation, thus prevented immunocompromise in restraint-stressed mice.

Dataset Information

Dataset describing maternal prenatal restraint stress effects on immune factors in mice.

Publications

Dataset describing maternal prenatal restraint stress effects on immune factors in mice.

Similar Datasets

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