We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Nanoplastics Chronic Toxicity in Mice: Disturbing the Homeostasis of Tryptophan Metabolism in Gut‐Lung‐Microbiota Axis
Summary
Researchers studied how long-term nanoplastic exposure affects mice and found it caused inflammation in the colon and scarring in lung tissue by disrupting a key amino acid metabolism pathway connecting the gut and lungs. They discovered that a beneficial gut bacterium called Akkermansia muciniphila was depleted after exposure, and restoring it helped reduce the damage. The study suggests that supporting healthy gut bacteria may be a strategy for mitigating the harmful effects of nanoplastic exposure.
Long-term exposure to nanoplastics causes chronic toxicity in mammals, particularly in the gut and lung tissues. The gut-lung-microbiota axis plays a pivotal role in organisms through the management of gut bacteria amino acid metabolic homeostasis. However, chronic toxicity of nanoplastics from gut to lungs have yet to be fully elucidated. In this study, nanoplastics exposure not only causes colon inflammation but also results in lung fibrosis. The abundance of Akkermansia muciniphila (AKK) is decreased after nanoplastics exposure. Interestingly, a positive correlation is observed between AKK and indole-3-lactic (ILA). Supplementation with AKK or ILA ameliorated nanoplastics-induced gut-derived lung injury by restoring the balance of tryptophan metabolism. Furthermore, knocking down indoleamine 2,3-dioxygenase 1 (ido1) upregulated ILA levels, contributing to defense against damage from nanoplastics. These results suggest that regulating ido1 expression and AKK abundance, involved in tryptophan metabolic homeostasis (especially ILA production), maybe a strategy to reduce the biological toxicity induced by nanoplastics. Mogroside V, a natural product, is found to promote AKK growth and inhibit ido1, thereby ameliorating chronic toxicity induced by nanoplastics. The study offers a new understanding of how nanoplastics cause chronic toxicity by dysregulating gut-lung-microbiota axis, as well as strategies for preventing and treating nanoplastics.
Sign in to start a discussion.
More Papers Like This
Gut-lung microbiota dynamics in mice exposed to Nanoplastics
Researchers gave mice PET nanoplastics orally for 28 days and analyzed the microbiome in their lungs, colon, mouth, and stool. While gut and oral bacteria were relatively unchanged, the lung microbiome showed significant shifts, including increases in bacteria associated with respiratory inflammation. The findings suggest a gut-lung connection where ingested nanoplastics may influence lung microbial communities even when gut bacteria appear unaffected.
Nanoplastics and triclosan co-exposure aggravates DSS-induced colitis in mice by interfering with Akkermansia muciniphila and tryptophan metabolism
Mouse colitis experiments showed that combined exposure to polystyrene nanoplastics and the antimicrobial triclosan worsened intestinal inflammation by depleting Akkermansia muciniphila and disrupting tryptophan metabolism, revealing synergistic gut-disrupting effects of these two common environmental pollutants.
Gut-lung axis: a novel mechanism involving microbiota dysbiosis-coordinated PLA2-TRPV1 neuroimmune crosstalk in nanoplastic-induced asthma exacerbation
Researchers found that inhaled polystyrene nanoplastics worsen asthma in mice by triggering a chain reaction involving gut bacteria disruption, nerve-immune signaling, and airway inflammation, revealing a gut-lung connection where plastic particles in the body can amplify respiratory disease through multiple biological pathways at once.
Lactate exacerbates lung damage induced by nanomicroplastic through the gut microbiota–HIF1a/PTBP1 pathway
Researchers found that nanoplastic exposure (particles 50–100 nm) disrupts gut bacteria in mice, causing lactate to build up in the lungs and triggering a cellular pathway that worsens lung damage through a process called epithelial-mesenchymal transition, where lung tissue changes in ways linked to scarring. The findings identify lactate and the gut-lung axis as key targets for preventing nanoplastic-induced lung injury.
Perturbation of gut microbiota plays an important role in micro/nanoplastics-induced gut barrier dysfunction
Researchers investigated how micro- and nanoplastics disrupt gut barrier function in mice, finding that different surface chemistries caused varying levels of damage. The study suggests that these plastic particles harm the gut by altering the gut microbiome, which then leads to inflammation and weakening of the intestinal barrier that normally keeps harmful substances out of the body.