Abstract

A growing body of evidence highlights that several insults during pregnancy impact the vascular function and immune response of the male and female offspring. Overactivation of the immune system negatively influences cardiovascular function and contributes to cardiovascular disease. In this review, we propose that modulation of the immune system is a potential link between prenatal stress and offspring vascular dysfunction. Glucocorticoids are key mediators of stress and modulate the inflammatory response. The potential mechanisms whereby prenatal stress negatively impacts vascular function in the offspring, including poor hypothalamic–pituitary–adrenal axis regulation of inflammatory response, activation of Th17 cells, renin–angiotensin–aldosterone system hyperactivation, reactive oxygen species imbalance, generation of neoantigens and TLR4 activation, are discussed. Alterations in the immune system by maternal stress during pregnancy have broad relevance for vascular dysfunction and immune-mediated diseases, such as cardiovascular disease.

Highlights

  • Fetal programming is characterized by environmental events experienced during fetal development, inducing immune and inflammatory consequences to the fetus along its lifespan (Facchi et al, 2020)

  • A growing body of evidence supports the idea that glucocorticoid-related genes involved in augmented cardiovascular risk factors in adult life are targeted by DNA methylation, resulting from early life stressful environment (Friso et al, 2008; Reynolds et al, 2013; Tobi et al, 2018)

  • The focus of this chapter is to connect the mechanisms of the immune response that contribute to vascular dysfunction and that can be programmed by maternal stress during pregnancy

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Summary

Introduction

Fetal programming is characterized by environmental events experienced during fetal development, inducing immune and inflammatory consequences to the fetus along its lifespan (Facchi et al, 2020). Stress induces different signaling pathways, the glucocorticoids are key mediators of stress response (Molnar et al, 2003; FIGURE 1 | Feedback between maternal stress-induced glucocorticoid production by HPA axis (hypothalamic–pituitary–adrenal axis) activation and fetal programming induced cardiometabolic disease in offspring adult.

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