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Long-term pathological consequences of prenatal infection: beyond brain disorders


Labouesse, Marie A; Langhans, Wolfgang; Meyer, Urs (2015). Long-term pathological consequences of prenatal infection: beyond brain disorders. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 309(1):R1-R12.

Abstract

Prenatal immunological adversities such as maternal infection have been widely acknowledged to contribute to an increased risk of neurodevelopmental brain disorders. In recent years, epidemiological and experimental evidence has accumulated to suggest that prenatal exposure to immune challenges can also negatively affect various physiological and metabolic functions beyond those typically associated with primary defects in CNS development. These peripheral changes include excessive accumulation of adipose tissue and increased body weight, impaired glycemic regulation and insulin resistance, altered myeloid lineage development, increased gut permeability, hyperpurinergia, and changes in microbiota composition. Experimental work in animal models further suggests that at least some of these peripheral abnormalities could directly contribute to CNS dysfunctions, so that normalization of peripheral pathologies could lead to an amelioration of behavioral deficits. Hence, seemingly unrelated central and peripheral effects of prenatal infection could represent interrelated pathological entities that emerge in response to a common developmental stressor. Targeting peripheral abnormalities may thus represent a valuable strategy to improve the wide spectrum of behavioral abnormalities that can emerge in subjects with prenatal infection histories.

Abstract

Prenatal immunological adversities such as maternal infection have been widely acknowledged to contribute to an increased risk of neurodevelopmental brain disorders. In recent years, epidemiological and experimental evidence has accumulated to suggest that prenatal exposure to immune challenges can also negatively affect various physiological and metabolic functions beyond those typically associated with primary defects in CNS development. These peripheral changes include excessive accumulation of adipose tissue and increased body weight, impaired glycemic regulation and insulin resistance, altered myeloid lineage development, increased gut permeability, hyperpurinergia, and changes in microbiota composition. Experimental work in animal models further suggests that at least some of these peripheral abnormalities could directly contribute to CNS dysfunctions, so that normalization of peripheral pathologies could lead to an amelioration of behavioral deficits. Hence, seemingly unrelated central and peripheral effects of prenatal infection could represent interrelated pathological entities that emerge in response to a common developmental stressor. Targeting peripheral abnormalities may thus represent a valuable strategy to improve the wide spectrum of behavioral abnormalities that can emerge in subjects with prenatal infection histories.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:05 Vetsuisse Faculty > Institute of Veterinary Pharmacology and Toxicology
Dewey Decimal Classification:570 Life sciences; biology
Language:English
Date:2015
Deposited On:03 Feb 2016 14:10
Last Modified:05 Apr 2016 19:59
Publisher:American Physiological Society
ISSN:0363-6119
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1152/ajpregu.00087.2015
PubMed ID:25924881

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