title: Maternal and early life stress effects on immune function: relevance to immunotoxicology.
abstract: Stress is triggered by a variety of unexpected environmental stimuli, such as aggressive behavior, fear, forced physical activity, sudden environmental changes, social isolation or pathological conditions. Stressful experiences during very early life (particularly, maternal stress during fetal ontogeny) can permanently alter the responsiveness of the nervous system, an effect called programming or imprinting. Programming affects the hypothalamic-pituitary-adrenocortical (HPA) axis, brain neurotransmitter systems, sympathetic nervous system (SNS), and the cognitive abilities of the offspring, which can alter neural regulation of immune function. Prenatal or early life stress may contribute to the maladaptive immune responses to stress that occur later in life. This review focuses on the effect of maternal and early life stress on immune function in the offspring across life span. It highlights potential mechanisms by which prenatal stress impacts immune functions over life span. The literature discussed in this review suggests that psychosocial stress during pre- and early postnatal life may increase the vulnerability of infants to the effects of immunotoxicants or immune-mediated diseases, with long-term consequences. Neural-immune interactions may provide an indirect route through which immunotoxicants affect the developing immune system. A developmental approach to understanding how immunotoxicants interact with maternal and early life stress-induced changes in immunity is needed, because as the body changes physiologically across life span so do the effects of stress and immunotoxicants. In early and late life, the immune system is more vulnerable to the effects of stress. Stress can mimic the effects of aging and exacerbate age-related changes in immune function. This is important because immune dysregulation in the elderly is more frequently and seriously associated with clinical impairment and death. Aging, exposure to teratogens, and psychological stress interact to increase vulnerability and put the elderly at the greatest risk for disease.
authors.affiliation: Department of Human Anatomy and Pathology, Loma Linda University School of Medicine, Loma Linda, CA 92352, USA. dbellinger@llu.edu
authors.forename: Denise L
authors.initials: DL
authors.lastname: Bellinger
authors.forename: Cheri
authors.initials: C
authors.lastname: Lubahn
authors.forename: Dianne
authors.initials: D
authors.lastname: Lorton
mesh_terms: D000818:Animals; D054750:Ecotoxicology; D005260:Female; D006801:Humans; D007107:Immune System / Q000196:embryology* / Q000254:growth & development / Q000503:physiopathology*; D008954:Models, Biological; D015213:Neuroimmunomodulation / Q000502:physiology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000209:etiology / Q000276:immunology; D013315:Stress, Psychological / Q000150:complications* / Q000276:immunology / Q000378:metabolism