Dataset Information

Maternal prenatal stress exposure and sex-specific risk of severe infection in offspring.

ABSTRACT:

Background

Maternal stressful life events during pregnancy have been associated with immune dysregulation and increased risk for asthma and atopy in offspring. Few studies have investigated whether prenatal stress is associated with increased overall or specific infectious diseases in childhood, nor explored sex differences. We sought to examine the relationship between the nature and timing of maternal stress in pregnancy and hospitalisation with infection in offspring.

Methods

Between 1989 and 1992, exposure data on stressful life events were collected from pregnant women (Gen1) in the Raine Study at 18 and 34 weeks' gestation and linked to statutory state-wide hospital morbidity data. We examined associations between the number, category and timing of maternal prenatal stress events and overall and clinical groups of offspring (Gen2) infection-related hospitalisation until age 16 years, adjusting for maternal age, education, and smoking in pregnancy in addition to the presence of siblings at birth.

Results

Of 2,141 offspring with complete stress in pregnancy data available, 1,089 had at least one infection-related hospitalisation, with upper respiratory tract infections the most common (n = 556). Each additional stressful life event during pregnancy was associated with increased risk in male offspring for hospitalisation with all infection types. There was little evidence of these associations in girls.

Conclusions

Increased exposure to stressful life events in utero is associated with sex-specific infection-related hospitalisations in childhood. Prenatal stress may adversely affect early immune development for boys and increase the risk of more severe infections. Mechanistic understanding would inform preventative interventions.

SUBMITTER: Robinson M

PROVIDER: S-EPMC7845992 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature

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Publications

Maternal prenatal stress exposure and sex-specific risk of severe infection in offspring.

Robinson Monique M Carter Kim W KW Pennell Craig E CE Jacoby Peter P Moore Hannah C HC Zubrick Stephen R SR Burgner David D

PloS one 20210129 1

<h4>Background</h4>Maternal stressful life events during pregnancy have been associated with immune dysregulation and increased risk for asthma and atopy in offspring. Few studies have investigated whether prenatal stress is associated with increased overall or specific infectious diseases in childhood, nor explored sex differences. We sought to examine the relationship between the nature and timing of maternal stress in pregnancy and hospitalisation with infection in offspring.<h4>Methods</h4>B ...[more]

PMID: 33513152

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Project description:ImportancePrenatal stress is associated with increased risks of several cardiovascular risk factors later in life. However, knowledge regarding the role of prenatal stress in the development of ischemic heart disease (IHD) and stroke is very limited.ObjectiveTo examine prenatal stress, defined as maternal bereavement, and risks of IHD and stroke in the offspring.Design, setting, and participantsA cohort study was conducted using data from Danish and Swedish registries. Live singleton births during calendar years 1973-2016 in Denmark (followed up until December 31, 2016) and during calendar years 1973-2014 in Sweden (followed up until December 31, 2021) were included in the analysis.ExposureMaternal loss of a close family member (partner, older children, parents, or siblings) the year before or during the pregnancy.Main outcome and measuresDiagnoses of IHD and stroke. Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% CIs for IHD and stroke in the offspring according to maternal bereavement.ResultsThe study included 6 758 560 births (39.4% from Denmark; 51.4% boys). During the median follow-up of 24.6 (IQR, 13.9-35.1) years, 8664 offspring (0.1%) were diagnosed with IHD and 13 094 with stroke (0.2%). Overall, maternal bereavement the year before or during pregnancy was not associated with IHD (adjusted HR [AHR], 0.98; 95% CI, 0.85-1.13) or stroke (AHR, 1.04; 95% CI, 0.94-1.16) in offspring. Similarly, no associations were observed when exposure was classified by the mother's relationship to the deceased individual, ie, loss of older child or partner (HR, 0.85; 95% CI, 0.64-1.14 for IHD and 0.98; 95% CI, 0.77-1.25 for stroke) or loss of parent or sibling (HR, 1.03; 95% CI, 0.87-1.21 for IHD and 1.06; 95% CI, 0.94-1.19 for stroke). However, associations between loss in the third trimester and IHD (AHR, 1.50; 95% CI, 1.06-2.13), and loss due to cardiovascular disease and stroke (AHR, 1.22; 95% CI, 1.03-1.44) were identified when exposure was classified by time of loss or the relative's cause of death.Conclusions and relevanceThe findings of this study provide little support for the hypothesis that prenatal stress is associated with risks of IHD and stroke in the first 5 decades of life. However, the association observed between stress in the third trimester and IHD warrants further investigation.

Project description:The prevalence of inflammatory bowel disease (IBD) is increasing worldwide and correlates with dysregulated immune response because of gut microbiota dysbiosis. Some adverse early life events influence the establishment of the gut microbiota and act as risk factors for IBD. Prenatal maternal stress (PNMS) induces gut dysbiosis and perturbs the neuroimmune network of offspring. In this study, we aimed to investigate whether PNMS increases the susceptibility of offspring to colitis in adulthood. The related index was assessed during the weaning period and adulthood. We found that PNMS impaired the intestinal epithelial cell proliferation, goblet cell and Paneth cell differentiation, and mucosal barrier function in 3-week-old offspring. PNMS induced low-grade intestinal inflammation, but no signs of microscopic inflammatory changes were observed. Although there was no pronounced difference between the PNMS and control offspring in terms of their overall measures of alpha diversity for the gut microbiota, distinct microbial community changes characterized by increases in Desulfovibrio, Streptococcus, and Enterococcus and decreases in Bifidobacterium and Blautia were induced in the 3-week-old PNMS offspring. Notably, the overgrowth of Desulfovibrio persisted from the weaning period to adulthood, consistent with the results observed using fluorescence in situ hybridization in the colon mucosa. Mechanistically, the fecal microbiota transplantation experiment showed that the gut microbiota from the PNMS group impaired the intestinal barrier function and induced low-grade inflammation. The fecal bacterial solution from the PNMS group was more potent than that from the control group in inducing inflammation and gut barrier disruption in CaCo-2 cells. After treatment with a TNF-α inhibitor (adalimumab), no statistical difference in the indicators of inflammation and intestinal barrier function was observed between the two groups. Finally, exposure to PNMS remarkably increased the values of the histopathological parameters and the inflammatory cytokine production in a mouse model of experimental colitis in adulthood. These findings suggest that PNMS can inhibit intestinal development, impair the barrier function, and cause gut dysbiosis characterized by the persistent overgrowth of Desulfovibrio in the offspring, resulting in exacerbated experimental colitis in adulthood.

Dataset Information

Maternal prenatal stress exposure and sex-specific risk of severe infection in offspring.

Background

Methods

Results

Conclusions

Publications

Maternal prenatal stress exposure and sex-specific risk of severe infection in offspring.

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