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Deleterious imprinting of perinatal exposure to nano-polystyrene on inflammatory bowel diseases
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Perinatal exposure to nano-polystyrene in mice produced long-lasting imprinting effects on inflammatory bowel disease susceptibility, with offspring showing heightened intestinal inflammation in adulthood. The study demonstrated that early-life plastic nanoparticle exposure can permanently alter immune system programming with consequences for chronic gut disease.
Abstract The tremendous and exponential production of plastics as well as its poor recycling leads to massive release in the environment questioning their outcomes on human health. Plastics are degraded into micro-plastic (MPL) and nano-plastic (NPL) that undergo weathering. MPL and NPL enter the human food chain via contaminated food, when animals are bred or vegetables grew on in plastic polluted environment and through the degradation of plastics food packaging. Ingested MPL or NPL can pass through epithelial barrier. This study focuses on consequences of oral perinatal exposure to polystyrene 50nm pristine or weathered (w) on intestinal disorders onset in offspring. Mouse were forced fed daily with 1.25mg of PS50 or PS50w starting at 15 days of gestation until pups weaned (Post Natal Day PND21). Oral tolerance protocol was induced at PND15 (nutritional switch) with ovalbumin (OVA) whereas DSS-induced colitis was performed in PND63 offspring. PS50 nor PS50w perinatal exposure did impair tolerance or immunization to OVA at PND15 in male or females. However, PS50 and PS50w perinatal exposure significantly worsened macroscopic score of DSS-induced colitis in both sexes. Perinatal exposure to PS50w appeared to be even more deleterious than PS50 for colitis exacerbation in males. In conclusion, early life exposure to PS50 or PS50w has long-lasting consequences on gut physiology by increasing the colonic severity of colitis while it does not modify oral tolerance establishment in early life. Those preliminary results questioned the kinetic of perinatal PS50 and PS50w exposure outcome over the life course and introduce the notion of imprinting. Highlights Perinatal exposure to PS50 or PS50w does not affect oral tolerance establishment nor immune response to immunisation at PND15 Perinatal exposure to PS50 or PS50w have long lasting consequences on intestinal inflammation and colitis. PS50w in male has even more deleterious outcomes. Restricted exposure to PS50 or PS50w during perinatal has a deleterious imprinting on adult offspring intestinal health Graphical abstract Environmental implication The use of plastics in daily products leads to ubiquitous contamination of the environment and subsequently of food chains. Plastics persist for long periods in the environment where, submitted to climate, they fragment into nanoplastic particles (NPL). Indeed, these NPL are weathered due to their exposure to UV light, thermal, chemical, physical and biological stresses. Thus, human populations are exposed to pristine (NPLp) and weathered NPL (NPLw) in their daily lives, with unknown effect on intestinal health, including the diseases development like adverse Food Reactions (AFR) or Inflammatory Bowel Diseases (IBD). Given that these pathologies could originate in perinatal development and that pregnant and breastfeeding women are exposed to NPL on a daily basis, this study explores the impact of perinatally exposure to pristine or weathered polystyrene nanoplastics on the gut development and susceptibility.
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Perinatal exposure to nano-polystyrene: deleterious imprinting on inflammatory bowel diseases
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When pregnant and nursing mice were fed tiny plastic particles (nanoplastics, like those found in our food and water), their offspring grew up with a higher risk of severe gut inflammation later in life, even though the exposure happened only early on. This suggests that plastic exposure during pregnancy and breastfeeding could set the stage for digestive diseases like colitis much later in life, raising concerns about how early-life plastic exposure might affect human gut health long-term.
Polystyrene micro- and nanoplastics in a colitis mouse model – effects on biodistribution, macrophage polarization, and gut microbiome
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Researchers exposed colitis mouse models to polystyrene micro- and nanoplastics to test whether MNP exposure worsens inflammatory bowel disease, finding that MNPs altered biodistribution and exacerbated inflammatory responses in animals with pre-existing gut inflammation.
Differently surface-labeled polystyrene nanoplastics at an environmentally relevant concentration induced Crohn’s ileitis-like features via triggering intestinal epithelial cell necroptosis
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Researchers found that polystyrene nanoplastics at environmentally realistic levels triggered Crohn's disease-like inflammation in the small intestine of mice. Different surface coatings on the nanoplastics affected which immune pathways were activated, but all types caused gut damage. This study suggests that nanoplastic exposure through food and water could contribute to inflammatory bowel disease in humans.
Intergenerational neurotoxicity of polystyrene nanoplastics in offspring mice is mediated by dysfunctional microbe-gut-brain axis
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Researchers found that mother mice exposed to polystyrene nanoplastics during pregnancy and nursing passed neurological harm to their offspring, with the babies showing brain inflammation, disrupted dopamine and serotonin signaling, and gut microbiome imbalances — suggesting that nanoplastic exposure before birth can damage the developing brain through the gut-brain connection.
Influence of Microplastics on Morphological Manifestations of Experimental Acute Colitis
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Researchers fed polystyrene microplastics to mice for six weeks and found that healthy mice developed changes in their colon lining, including altered mucus composition and immune cell populations. When mice with experimentally induced colitis also consumed microplastics, their intestinal inflammation was significantly more severe. The study suggests that microplastic exposure may worsen inflammatory bowel conditions.
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