Prenatal maternal stress predicts reductions in CD4+ lymphocytes, increases in innate-derived cytokines, and a Th2 shift in adolescents: Project Ice Storm

Veru, Franz; Dancause, Kelsey Needham; Laplante, David P.; King, Suzanne; Luheshi, Giamal N.

doi:10.1016/j.physbeh.2015.03.016

Cited by 66 publications

(53 citation statements)

References 52 publications

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“…It was reported that prenatal tetrachlorodibenzo-p-dioxin (TCDD) exposure could increase the IL-4 production of splenic immune cells in male offspring40. In addition, prenatal maternal stress could enhance the Th2 cytokines IL-4 and IL-1341. Furthermore, mice immunized with OVA mounted strong Th2 responses as indicated by the significant level of IL-4 and undetectable level of IFN-γ42.…”

Section: Discussionmentioning

confidence: 99%

Increased Fetal Thymocytes Apoptosis Contributes to Prenatal Nicotine Exposure-induced Th1/Th2 Imbalance in Male Offspring Mice

Chen

Yan

et al. 2016

Sci Rep

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Nicotine, a definite risk factor during pregnancy, is an immunomodulator. This study was designed to investigate the effects of prenatal nicotine exposure (PNE) on the balance of Th1/Th2 in offspring, and further explore the developmental origin mechanisms from the perspective of fetal thymocytes apoptosis. Pregnant Balb/c mice were administered 1.5 mg/kg nicotine subcutaneously twice per day from gestational day (GD) 9 to GD18. Results showed that PNE could cause a Th2 shift in male offspring, manifested as increased ratio of IgG1/IgG2a, IL-4 production in serum, and IL-4/IFN-γ expression ratio in spleen. Increased apoptosis of total thymocytes and CD4SP and reduced cell proportion of CD4SP were found in PNE male offspring on postnatal day (PND) 14 and PND 49. In the fetuses, decreased body weight and organ index of fetal thymus, histological changes in fetal thymus, reduced CD4SP proportion and increased fetal thymocyte apoptosis were observed in nicotine group. The increased mRNA expression of genes involved in Fas-mediated apoptotic pathway and protein expression of Fas were also detected. In conclusion, PNE could cause a Th2 shift in male offspring mediated by reduced CD4+ T cells output, which may result from the increasing apoptosis of total thymocytes and CD4SP.

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Section: Discussionmentioning

confidence: 99%

Increased Fetal Thymocytes Apoptosis Contributes to Prenatal Nicotine Exposure-induced Th1/Th2 Imbalance in Male Offspring Mice

Chen

Yan

et al. 2016

Sci Rep

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“…Animal studies showed that stress during pregnancy can activate the foetal hypothalamic‐pituitary‐adrenal axis and sympathetic adrenomedullary system leading to sustained excessive glucocorticoids and catecholamines levels, respectively . Glucocorticoids and catecholamines may induce a type 2 T‐helper (Th2) cell predominance leading to increased secretion of pro‐inflammatory and Th2 cytokines . This may promote immunoglobulin E (IgE) production and, subsequently, atopic inflammation and diseases .…”

Section: Introductionmentioning

confidence: 99%

Maternal psychiatric symptoms during pregnancy and risk of childhood atopic diseases

Elbert

Duijts

Dekker

et al. 2017

Clin Experimental Allergy

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SummaryBackground Maternal psychiatric symptoms during pregnancy might affect the developing immune system and subsequent risk of childhood atopic diseases. Objective Our aim was to examine the associations of maternal psychiatric symptoms during pregnancy with allergic sensitization, allergy and eczema in children until age 10 years. Methods This study among 5205 children was performed in a population-based prospective cohort from foetal life onwards. We assessed maternal and paternal psychiatric symptoms (overall, depressive, anxiety) during pregnancy and at 36 months after delivery, and maternal psychiatric symptoms at 2 and 6 months after delivery using the Brief Symptom Inventory. Inhalant and food allergic sensitization were measured by skin prick tests, and physician-diagnosed inhalant and food allergy or eczema by questionnaires from birth until age 10 years. We used multivariate logistic regression, multinomial logistic regression or generalized estimating equation models where appropriate. Results We observed no association of maternal psychiatric symptoms during pregnancy with allergic sensitization. Maternal overall psychiatric, depressive and anxiety symptoms during pregnancy were associated with an increased risk of inhalant allergy only (adjusted odds ratio (95% confidence interval) 1.96 (1.44, 2.65), 1.58 (1.25, 1.98) and 1.61 (1.27, 2.03), respectively, per 1-unit increase). Maternal overall psychiatric and anxiety symptoms during pregnancy were associated with an increased risk of eczema (1.21 (1.05, 1.39) and 1.15 (1.02, 1.29), respectively, per 1-unit increase). Effect estimates did not materially change when maternal psychiatric symptoms after delivery, or paternal psychiatric symptoms during pregnancy and after delivery were taken into account. Conclusions and Clinical Relevance Maternal psychiatric symptoms during pregnancy were associated with increased risks of childhood inhalant allergy and eczema, independent of maternal psychiatric symptoms after delivery and of paternal psychiatric symptoms.

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“…In human studies, stressors during pregnancy are associated with altered concentrations of inflammatory biomarkers in maternal circulation, greater expression of pro‐inflammatory transcripts in the placenta, and over‐production of pro‐inflammatory cytokines by immune cells in response to immunostimulants (Borders et al, ; Coussons‐Read, Okun, & Nettles, ; Ernst et al, ; Gilman et al, ; Miller et al, ). The reported cytokine responses depend on the type and timing of the prenatal stressor, with elevated levels of IL‐6 and CRP most commonly reported (Bronson & Bale, ; Coussons‐Read et al, ; Veru, Dancause, Laplante, King, & Luheshi, ) and more recently decreased levels of IL‐8 (Gilman et al, ).…”

Section: Non‐infectious Models Of Miamentioning

confidence: 99%

Maternal immune activation, central nervous system development and behavioral phenotypes

Minakova

Warner

2018

Birth Defects Research

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Maternal immune activation (MIA) refers to a maternal immune system triggered by infectious or infectious-like stimuli. A cascade of cytokines and immunologic alterations are transmitted to the fetus, resulting in adverse phenotypes most notably in the central nervous system. Epidemiologic studies implicate maternal infections in a variety of neuropsychiatric disorders, most commonly autism spectrum disorders and schizophrenia. In animal models, MIA causes neurochemical and anatomic changes in the brain that correspond to those found in humans with the disorders. As our understanding of the interactions between environment, genetics, and immune system grows, the role of alternative, noninfectious risk factors, such as prenatal stress, obesity, and the gut microbiome also becomes clearer. This review considers how infectious and noninfectious etiologies activate the maternal immune system. Their impact on fetal programming and neuropsychiatric disorders in offspring is examined in the context of human and animal studies.

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Prenatal maternal stress predicts reductions in CD4+ lymphocytes, increases in innate-derived cytokines, and a Th2 shift in adolescents: Project Ice Storm

Cited by 66 publications

References 52 publications

Increased Fetal Thymocytes Apoptosis Contributes to Prenatal Nicotine Exposure-induced Th1/Th2 Imbalance in Male Offspring Mice

Increased Fetal Thymocytes Apoptosis Contributes to Prenatal Nicotine Exposure-induced Th1/Th2 Imbalance in Male Offspring Mice

Maternal psychiatric symptoms during pregnancy and risk of childhood atopic diseases

Maternal immune activation, central nervous system development and behavioral phenotypes

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