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Lactate exacerbates lung damage induced by nano-microplastics through the gut microbiota–HIF1a/PTBP1 pathway
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A new study found that tiny plastic particles (nano-microplastics) can disrupt the gut bacteria in mice, causing a buildup of lactate (a natural body chemical) that then travels through a specific biological pathway to worsen lung damage. This suggests that swallowing microplastics, now common in food, water, and even the air we breathe, might harm your lungs indirectly by first messing with your gut health, highlighting yet another reason to be concerned about everyday plastic exposure.
We read and had great interest in the article written by Xuan et al. 1 . This study revealed that mice exhibited lung and intestinal mucosal damage, gut microbiota dysbiosis, and elevated lactate and N-cadherin levels after 28 days of exposure to nano-microplastics. In addition, lactate accumulation was strongly associated with an imbalance in lactic acid bacteria in the gut. Furthermore, no lactate accumulation was observed in germ-free mice, while depletion of the gut microbiota using a cocktail of antibiotics produced similar results. Mechanistically, elevated lactate level trigger activation of the HIF1a/PTBP1 pathway, which exacerbates nano-microplastic-induced lung damage through modulation of the epithelial–mesenchymal transition (EMT). However, we would like to discuss this topic further.
More Papers Like This
Lactate exacerbates lung damage induced by nanomicroplastic through the gut microbiota–HIF1a/PTBP1 pathway
AI summary Read the abstract
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.
Causal relationship between micro- and nanoplastics and lung function
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Researchers quantified micro- and nanoplastic levels in whole blood from young adults using pyrolysis GC-MS and measured lung function by spirometry, analyzing the causal relationship between circulating plastic particle burden and forced expiratory volume and vital capacity outcomes.
Polyethylene Microplastics Disrupt Cardiopulmonary Homeostasis via Oxidative Stress, Inflammatory Crosstalk, and Mitochondrial Dysfunction in Wistar Rats
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Male Wistar rats orally dosed with polyethylene microplastics for 28 days showed elevated cardiac and pulmonary injury biomarkers, suppressed antioxidant defenses, inhibited mitochondrial TCA cycle enzymes, and disrupted respiratory chain complexes, indicating simultaneous heart and lung damage through shared oxidative and inflammatory pathways. The study suggests that routine microplastic ingestion may impose systemic cardiopulmonary stress, with organ-specific dose-response differences suggesting the lungs may be particularly sensitive.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.