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Developmental exposure to polychlorinated biphenyls (PCBs) in the maternal diet
causes host-microbe defects in weanling offspring mice.
Rude KM, Pusceddu MM, Keogh CE, Sladek JA, Rabasa G, Miller EN, Sethi S, Keil
KP, Pessah IN, Lein PJ, Gareau MG
Submitted Externally on 9/26/2019
Environmental pollution (Barking, Essex : 1987)
Volume : Pages
253 : 708 - 721
The gut microbiota is important for maintaining homeostasis of the host. Gut
microbes represent the initial site for toxicant processing following dietary
exposures to environmental contaminants. The diet is the primary route of
exposure to polychlorinated biphenyls (PCBs), which are absorbed via the gut,
and subsequently interfere with neurodevelopment and behavior. Developmental
exposures to PCBs have been linked to increased risk of neurodevelopmental
disorders (NDD), including autism spectrum disorder (ASD), which are also
associated with a high prevalence of gastrointestinal (GI) distress and
intestinal dysbiosis. We hypothesized that developmental PCB exposure impacts
colonization of the gut microbiota, resulting in GI pathophysiology, in a
genetically susceptible host. Mouse dams expressing two heritable human
mutations (double mutants [DM]) that result in abnormal Ca2+ dynamics and
produce behavioral deficits (gain of function mutation in the ryanodine receptor
1 [T4826I-RYR1] and a human CGG repeat expansion [170-200 CGG repeats] in the
fragile X mental retardation gene 1 [FMR1 premutation]). DM and congenic wild
type (WT) controls were exposed to PCBs (0-6?mg/kg/d) in the diet starting 2
weeks before gestation and continuing through postnatal day 21 (P21). Intestinal
physiology (Ussing chambers), inflammation (qPCR) and gut microbiome (16S
sequencing) studies were performed in offspring mice (P28-P30). Developmental
exposure to PCBs in the maternal diet caused significant mucosal barrier defects
in ileum and colon (increased secretory state and tight junction permeability)
of juvenile DM mice. Furthermore, PCB exposure increased the intestinal
inflammatory profile (Il6, Il1ß, and Il22), and resulted in dysbiosis of the gut
microbiota, including altered ß-diversity, in juvenile DM mice developmentally
exposed to 1?mg/kg/d PCBs when compared to WT controls. Collectively, these
findings demonstrate a novel interaction between PCB exposure and the gut
microbiota in a genetically susceptible host that provide novel insight into
environmental risk factors for neurodevelopmental disorders.
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Financial support for this work was provided by the NIDDK Mouse Metabolic Phenotyping Centers (National MMPC, RRID:SCR_008997,
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