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Micro-nanoplastics inhibit extracellular polymeric substance and lactate synthesis via perturbing glucose metabolism of Lacticaseibacillus rhamnosus
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Researchers found that micro- and nanoplastics — especially nanoscale PET particles — impair the probiotic bacterium Lactobacillus rhamnosus by disrupting central carbon metabolism, reducing its production of lactic acid and protective extracellular polysaccharides, raising concerns that microplastic ingestion could compromise the gut benefits of probiotic bacteria.
Micro-nanoplastics (MNPs) ubiquitously occurring in various ecosystems can accumulate in the human gastrointestinal tract via multiple exposure routes, and threaten the intestinal homeostasis. However, clarifying whether and how these contaminants cause the physio-toxicity to intestinal probiotics remains elusive. Using Lacticaseibacillus rhamnosus as a case study and an in vitro digestion (IVD) system to simulate MNPs digestion, we found that MNPs inhibit bacterial growth and the synthesis of extracellular polymeric substances (EPS) and lactic acid (LA). This toxicity depended on material composition (polyethylene terephthalate, PET > polystyrene > polyvinyl chloride), was enhanced at the nanoscale, and was exacerbated by high concentrations. Under the strongest inhibitory condition (150.0 nm 250.0 mg/L IVD-treated PET; PET-NPs), scanning electron microscopy reveals that EPS secreted by L. rhamnosus under PET-NPs stimulation binds to the particles and adheres to the bacterial surface, potentially causing physical obstruction and membrane damage. Integrated transcriptomics and metabolomics demonstrated that IVD-treated PET-NPs significantly down-regulated core genes (e.g., galK, logFC = -5.40; bglA, logFC = -6.58), and reduced metabolite levels in central carbon metabolism pathways (e.g., phosphotransferase system, glycolysis, TCA cycle, pentose phosphate pathway, oxidative phosphorylation), impairing glucose uptake/metabolism and energy generation, and thus limiting precursor supply for EPS and LA synthesis. Although exogenous glucose partially restored function, upstream metabolic damage persisted. The findings indicate that MNPs disrupt the glucose metabolism-product synthesis axis by inhibiting central carbon metabolism, providing clear evidence of MNP-mediated impairment of metabolism and efficacy in probiotics and mechanistic insights into the potential health impacts of MNPs contaminants.
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