Childhood exposure to tobacco and mercury: gut microbiota
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB69271 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12265300_1.fastq.gz | Fastqsanger.gz | |||
| ERR12265300_2.fastq.gz | Fastqsanger.gz | |||
| ERR12265301_1.fastq.gz | Fastqsanger.gz | |||
| ERR12265301_2.fastq.gz | Fastqsanger.gz | |||
| ERR12265302_1.fastq.gz | Fastqsanger.gz |
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Project description:Exposure to secondhand tobacco smoke during early childhood has been linked with an increased risk for behavioral disorders, yet little is known regarding how brain development is impacted. Using an environmental tobacco smoke (ETS) passive inhalation model, this study assesses the neurodevelopmental impact of juvenile exposure during a critical period of frontal cortex development, specifically that of the rat orbital neocortex between postnatal days 8 and 22. Agnostic shotgun proteomics was employed to discern the biomolecular shift within this rapidly developing brain region that is responsible for higher-order behavioral control. The orbital cortex neuroproteome was assessed between ETS-exposed and room-air control animals employing a label-free shotgun approach with data-independent acquisition. Following protein roll-up, a total of X protein were found statistically altered in quantity out of Y total proteins identified. These results implicate a prominent shift within metabolic processes and synaptic organization related to excitatory and inhibitory neurotransmission. Findings derived from this dataset may further our understanding of how secondhand smoke exposure can perturb the orbital frontal cortex and result in developmental behavioral disorders.
2018-12-17 | PXD011744 | Pride
Project description:Exposure to secondhand tobacco smoke during early childhood has been linked with an increased risk for behavioral disorders, yet little is known regarding how brain development is impacted. Using an environmental tobacco smoke (ETS) passive inhalation model, this study assesses the neurodevelopmental impact of juvenile exposure during a critical period of frontal cortex development, specifically that of the rat orbital neocortex between postnatal days 8 and 22. Agnostic shotgun proteomics was employed to discern the biomolecular shift within this rapidly developing brain region that is responsible for higher-order behavioral control. The orbital cortex neuroproteome was assessed between ETS-exposed and room-air control animals employing a label-free shotgun approach with data-independent acquisition. Following protein roll-up, a total of X protein were found statistically altered in quantity out of Y total proteins identified. These results implicate a prominent shift within metabolic processes and synaptic organization related to excitatory and inhibitory neurotransmission. Findings derived from this dataset may further our understanding of how secondhand smoke exposure can perturb the orbital frontal cortex and result in developmental behavioral disorders.
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Project description:BackgroundEarly life determinants of the development of gut microbiome composition in infants have been widely investigated; however, if early life pollutant exposures, such as tobacco or mercury, have a persistent influence on the gut microbial community, its stabilization at later childhood remains largely unknown.ObjectiveIn this exposome-wide study, we aimed at identifying the contribution of exposure to tobacco and mercury from the prenatal period to childhood, to individual differences in the fecal microbiome composition of 7-year-old children, considering co-exposure to a width of established lifestyle and clinical determinants.MethodsGut microbiome was studied by 16S rRNA amplicon sequencing in 151 children at the genus level. Exposure to tobacco was quantified during pregnancy through questionnaire (active tobacco consumption, second-hand smoking -SHS) and biomonitoring (urinary cotinine) at 4 years (urinary cotinine, SHS) and 7 years (SHS). Exposure to mercury was quantified during pregnancy (cord blood) and at 4 years (hair). Forty nine other potential environmental determinants (12 at pregnancy/birth/infancy, 15 at 4 years and 22 at 7 years, such as diet, demographics, quality of living/social environment, and clinical records) were registered. We used multiple models to determine microbiome associations with pollutants including multi-determinant multivariate analysis of variance and linear correlations (wUnifrac, Bray-Curtis and Aitchison ß-diversity distances), single-pollutant permutational multivariate analysis of variance adjusting for co-variates (Aitchison), and multivariable association model with single taxa (MaAsLin2; genus). Sensitivity analysis was performed including genetic data in a subset of 107 children.ResultsActive smoking in pregnancy was systematically associated with microbiome composition and ß-diversity (R2 2-4%, p < 0.05, Aitchison), independently of other co-determinants. However, in the adjusted single pollutant models (PERMANOVA), we did not find any significant association. An increased relative abundance of Dorea and decreased relative abundance of Akkermansia were associated with smoking during pregnancy (q < 0.05).DiscussionOur findings suggest a long-term sustainable effect of prenatal tobacco exposure on the children's gut microbiota. This effect was not found for mercury exposure or tobacco exposure during childhood. Assessing the role of these exposures on the children's microbiota, considering multiple environmental factors, should be further investigated.
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