Prenatal Stress and Immune Recognition of Self and Nonself in the Primate Neonate

Coe, Christopher L.; Lubach, Gabriele R.; Karaszewski, Joseph W.

doi:10.1159/000014172

Cited by 82 publications

(52 citation statements)

References 21 publications

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“…Moreover, in animal studies, gestational exposure to maternal stress alters the development of immunocompetence in offspring. Evidence in rhesus monkeys links prenatal stress to antigen-induced responses at birth (22). Dysregulated immune response to antigen challenge has also been demonstrated in prenatally stressed adult mice, reflected by an enhanced Th2 adaptive response (23).…”

Section: What This Study Adds To the Fieldmentioning

confidence: 99%

Prenatal Maternal Stress and Cord Blood Innate and Adaptive Cytokine Responses in an Inner-City Cohort

Wright¹,

Visness²,

Calatroni³

et al. 2010

Am J Respir Crit Care Med

204

157

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Rationale: Stress-elicited disruption of immunity begins in utero. Objectives: Associations among prenatal maternal stress and cord blood mononuclear cell (CBMC) cytokine responses were prospectively examined in the Urban Environment and Childhood Asthma Study (n 5 557 families). Methods: Prenatal maternal stress included financial hardship, difficult life circumstances, community violence, and neighborhood/block and housing conditions. Factor analysis produced latent variables representing three contexts: individual stressors and ecological-level strains (housing problems and neighborhood problems), which were combined to create a composite cumulative stress indicator. CBMCs were incubated with innate (lipopolysaccharide, polyinosinic-polycytidylic acid, cytosine-phosphate-guanine dinucleotides, peptidoglycan) and adaptive (tetanus, dust mite, cockroach) stimuli, respiratory syncytial virus, phytohemagglutinin, or medium alone. Cytokines were measured using multiplex ELISAs. Using linear regression, associations among increasing cumulative stress and cytokine responses were examined, adjusting for sociodemographic factors, parity, season of birth, maternal asthma and steroid use, and potential pathway variables (prenatal smoking, birth weight for gestational age). Measurements and Main Results: Mothers were primarily minorities (Black [71%], Latino [19%]) with an income less than $15,000 (69%). Mothers with the highest cumulative stress were older and more likely to have asthma and deliver lower birth weight infants. Higher prenatal stress was related to increased IL-8 production after microbial (CpG, PIC, peptidoglycan) stimuli and increased tumor necrosis factor-a to microbial stimuli (CpG, PIC). In the adaptive panel, higher stress was associated with increased IL-13 after dust mite stimulation and reduced phytohemagglutinin-induced IFN-g. Conclusions: Prenatal stress was associated with altered innate and adaptive immune responses in CBMCs. Stress-induced perinatal immunomodulation may impact the expression of allergic disease in these children.

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Section: What This Study Adds To the Fieldmentioning

confidence: 99%

Prenatal Maternal Stress and Cord Blood Innate and Adaptive Cytokine Responses in an Inner-City Cohort

Wright¹,

Visness²,

Calatroni³

et al. 2010

Am J Respir Crit Care Med

204

157

View full text Add to dashboard Cite

show abstract

“…Perinatal stress and long-term changes to the HPA axis Numerous animal models have demonstrated associations between prenatal stress and long-term alterations in HPA axis function (Coe et al, 1996(Coe et al, , 1999Kapoor et al, 2006;Weinstock, 2005). Healthy young adult humans who had been exposed to prenatal stress, because their mothers had experienced severe negative life events during pregnancy, responded differently to a standardized social stressor (TSST) when compared to an age-matched comparison group of healthy young adults who had not been exposed to prenatal stress.…”

Section: 2mentioning

confidence: 99%

Hygiene and Other Early Childhood Influences on the Subsequent Function of the Immune System

Rook

2012

Immunity to Parasitic Infection

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Hygiene Depression a b s t r a c tThe immune system influences brain development and function. Hygiene and other early childhood influences impact the subsequent function of the immune system during adulthood, with consequences for vulnerability to neurodevelopmental and psychiatric disorders. Inflammatory events during pregnancy can act directly to cause developmental problems in the central nervous system (CNS) that have been implicated in schizophrenia and autism. The immune system also acts indirectly by "farming" the intestinal microbiota, which then influences brain development and function via the multiple pathways that constitute the gut-brain axis. The gut microbiota also regulates the immune system.Regulation of the immune system is crucial because inflammatory states in pregnancy need to be limited, and throughout life inflammation needs to be terminated completely when not required; for example, persistently raised levels of background inflammation during adulthood (in the presence or absence of a clinically apparent inflammatory stimulus) correlate with an increased risk of depression. A number of factors in the perinatal period, notably immigration from rural low-income to rich developed settings, caesarean delivery, breastfeeding and antibiotic abuse have profound effects on the microbiota and on immunoregulation during early life that persist into adulthood. Many aspects of the modern western environment deprive the infant of the immunoregulatory organisms with which humans co-evolved, while encouraging exposure to nonimmunoregulatory organisms, associated with more recently evolved "crowd" infections.

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“…Animal studies suggest effects begin prenatally. Prenatal stress increases allergen-induced airway inflammation (10,11) and airway hyperesponsiveness (12) in mice offspring and impacts the newborn's antigen response in primates (13). Although no prospective human study has measured prenatal maternal stress directly in association with wheeze or other early asthma phenotypes in children, three have considered maternal psychologic functioning as a correlate of stress exposure.…”

mentioning

confidence: 99%

Prenatal and Postnatal Maternal Stress and Wheeze in Urban Children

Chiu¹,

Coull

Cohen

et al. 2012

Am J Respir Crit Care Med

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Rationale: Critical periods for programming early wheeze risk may include pregnancy and infancy. Effects of timing remain poorly understood. Objectives: Associations among prenatal and postnatal maternal stress and children's wheeze were prospectively examined in 653 families. Effect modification by maternal sensitization was also examined. Methods: Stress was indexed by a maternal negative life events (NLEs) score (range, 0-9) ascertained during pregnancy and between 1 and 2 years postpartum. Mothers reported child wheeze every 3 months up to age 2 years. Relationships of prenatal and postnatal maternal NLEs with repeated wheeze (>2 episodes) were examined using logistic regression adjusting for covariates. Penalized splines were implemented to explore possible nonlinear associations. We also examined the interaction between prenatal stress and maternal sensitization indexed by allergen-specific IgE from maternal prenatal serum. Measurements and Main Results: Adjusted models considering prenatal or postnatal NLEs alone both showed an exposure-response relationship between higher stress and child wheeze. When considering prenatal and postnatal stress concurrently, only children of mothers with high stress in both periods were significantly more likely to wheeze (adjusted odds ratio, 3.04; 95% confidence interval, 1.67-5.53) than children of mothers reporting low stress in both periods. Associations between high prenatal stress and wheeze were significant in children born to nonsensitized mothers (any IgE ,0.35 kU/L) but not in the sensitized group (P for interaction ¼ 0.03). Conclusions: Although children have heightened sensitivity to maternal stress in utero and in early childhood, those with higher stress in both periods were particularly at risk for wheeze. The prenatal maternal immune milieu modified effects.Keywords: negative life events; stress; pregnancy; maternal sensitization; childhood wheeze Childhood wheezing illnesses account for significant morbidity and health care use (1). Recurrent wheeze may be a precedent of asthma and reduced lung function (2). An important step in identifying children at risk for costly respiratory disorders is characterizing risk factors and mechanisms that lead to and maintain early predisposition.Although the spectrum of wheeze phenotypes is complex and mechanisms of early environmental influences are incompletely understood (3, 4), aberrant proinflammatory states are central determinants (5, 6). Glucocorticoid action and sympathovagal balance are important in regulating immune function and airway response in early development (7,8). Thus, environmental factors, such as psychosocial stressors, that influence the programming of regulatory systems involved in these processes (i.e., hypothalamic-pituitary-adrenal [HPA] axis, autonomic nervous system, immune function) may be particularly relevant.Evidence links psychosocial stress to wheeze, asthma, and airway hyperesponsiveness (9). Animal studies suggest effects begin prenatally. Prenatal stress increases allergen-induced ...

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Prenatal Stress and Immune Recognition of Self and Nonself in the Primate Neonate

Cited by 82 publications

References 21 publications

Prenatal Maternal Stress and Cord Blood Innate and Adaptive Cytokine Responses in an Inner-City Cohort

Prenatal Maternal Stress and Cord Blood Innate and Adaptive Cytokine Responses in an Inner-City Cohort

Hygiene and Other Early Childhood Influences on the Subsequent Function of the Immune System

Prenatal and Postnatal Maternal Stress and Wheeze in Urban Children

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