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

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology Vol. 309; no. 1; pp. R1 - R12
• Main Authors: Labouesse, Marie A., Langhans, Wolfgang, Meyer, Urs
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.07.2015
• Subjects: Adipose tissue; Adiposity; Age Factors; Animal models; Animals; Bacteria - immunology; Bacteria - pathogenicity; Body Weight; Brain diseases; Central Nervous System - immunology; Central Nervous System - microbiology; Central Nervous System - physiopathology; Communicable Diseases - complications; Communicable Diseases - immunology; Communicable Diseases - microbiology; Communicable Diseases - physiopathology; Dysbiosis; Energy Metabolism; Female; Gastrointestinal Tract - microbiology; Host-Pathogen Interactions; Humans; Immunology; Inflammation Mediators - metabolism; Metabolism; Pathology; Physiology; Pregnancy; Pregnancy Complications, Infectious - immunology; Pregnancy Complications, Infectious - microbiology; Pregnancy Complications, Infectious - physiopathology; Prenatal development; Prenatal Exposure Delayed Effects; Risk Factors; Signal Transduction; Time Factors; metabolic syndrome; maternal immune activation; cytokines; schizophrenia; autism; gut microbiota
• ISSN: 0363-6119; 1522-1490; 1522-1490
• DOI: 10.1152/ajpregu.00087.2015

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.