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Data from three prospective longitudinal human cohorts of prenatal marijuana exposure and offspring outcomes from the fetal period through young adulthood.

ABSTRACT: This article includes data from three prospective longitudinal human cohorts of prenatal marijuana exposure (PME) and offspring outcomes from the fetal period through young adulthood. The table herein contains an overview of the major adverse effects associated with PME from the following human cohorts: (1) The Ottawa Prenatal Prospective Study (OPPS); (2) The Maternal Health Practices and Child Development Study (MHPCD); and (3) The Generation R Study (Gen R). In the OPPS, fetal gestational age was measured and age-appropriate standardized neuropsychological instruments were used to assess neonatal responses, and infant-child and adolescent-young adult cognitive and behavioral skills. In the MHPCD, birth length and weight, neonatal body length, and infant-child sleep, cognition, and behavioral parameters were measured. In the Gen R, birth weight and growth were measured, as were infant-child attention and aggression. The data in this article are in support of our report entitled "Prenatal Cannabis Exposure - The "First Hit" to the Endocannabinoid System" (K.A. Richardson, A.K. Hester, G.L. McLemore, 2016) [13].

SUBMITTER: McLemore GL

PROVIDER: S-EPMC5096595 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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Data from three prospective longitudinal human cohorts of prenatal marijuana exposure and offspring outcomes from the fetal period through young adulthood.

McLemore Gabrielle L GL Richardson Kimberlei A KA

Data in brief 20161018

This article includes data from three prospective longitudinal human cohorts of prenatal marijuana exposure (PME) and offspring outcomes from the fetal period through young adulthood. The table herein contains an overview of the major adverse effects associated with PME from the following human cohorts: (1) The Ottawa Prenatal Prospective Study (OPPS); (2) The Maternal Health Practices and Child Development Study (MHPCD); and (3) The Generation R Study (Gen R). In the OPPS, fetal gestational age ...[more]

PMID: 27833935

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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

Data from three prospective longitudinal human cohorts of prenatal marijuana exposure and offspring outcomes from the fetal period through young adulthood.

Publications

Data from three prospective longitudinal human cohorts of prenatal marijuana exposure and offspring outcomes from the fetal period through young adulthood.

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