Abstract

The body is colonized by an enormous array of microbes that are collectively called the microbiota. During quiescent periods, microbial communities within the gut are relatively resistant to change. However, several factors that disrupt homeostasis can also significantly change gut microbial community structure. One factor that has been shown to change the composition of the gut microbiota is exposure to psychological stressors. Studies demonstrate that the commensal microbiota are involved in stressor-induced immunomodulation, but other biological effects are not yet known. This review discusses emerging evidence that the microbiota can impact the brain and behavior and indicates that stressor-induced alterations in the composition of gut microbial communities contribute to stressor-induced behavioral changes. This review will also discuss the evidence that such effects are most evident early in life, where both stress and the microbiota have been linked to birth outcomes, such as prematurity, and neurodevelopment. When considered together, a paradigm emerges in which stressor-induced alterations in commensal microbial populations significantly impact parturition and infant neurodevelopment.

Highlights

  • The hypothesis that the origins of adult disease are developmental, beginning in utero is called the “Barker hypothesis” after one of its leading proponents and the author of a study demonstrating increased risk of cardiovascular disease in infants born underweight [1]. It states that adverse influences early in development, such as poor nutrition or infection, result in permanent physiological changes and in increased disease risk in adulthood. This is an area of increasing research in many fields, including Psychiatry, Immunology, and Endocrinology, which are exploring whether development of diseases such as asthma, diabetes, and anxiety contains a developmental, intrauterine element

  • Neurodevelopment is exquisitely sensitive to perturbations in the maternal milieu, including diet, infection, and stress, with potentially longlasting behavioral consequences

  • STRESS, THE MICROBIOME, AND PRETERM BIRTH While it is becoming increasing evident that stressor-induced alterations in the microbiota of adult animals can significantly impact host physiology, these effects are transient and return to baseline after termination of the stressor

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Summary

Introduction

The hypothesis that the origins of adult disease are developmental, beginning in utero is called the “Barker hypothesis” after one of its leading proponents and the author of a study demonstrating increased risk of cardiovascular disease in infants born underweight [1]. While alterations in the hypothalamic–pituitary–adrenal (HPA) axis and immune function have been the target of investigation as underlying mechanisms conferring increased risk, the microbiome is an emerging candidate as a potential mediator of stress-induced pathogenesis (Figure 1). Studies from this laboratory, as well as others, have demonstrated that psychosocial stressors can impact microbial community structure in the gut.

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