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Trojan Horse Effect of Biologically Aged Microplastics-An Intracellular Carrier of LPS for Licensing Noncanonical Inflammasome Activation
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Researchers aged polystyrene microplastics biologically inside tissue and found the particles accumulated lipopolysaccharide (LPS) from bacteria; they then showed these biologically-aged particles could deliver LPS into cells to activate the non-canonical inflammasome pathway. This "Trojan horse" mechanism—absent with pristine or briefly-aged particles—suggests long-term tissue-trapped microplastics may trigger chronic inflammatory disease.
Microplastics (MPs), due to their poor degradability, can accumulate in the body following ingestion. Most studies evaluating MP safety use pristine particles or those aged for a short period, thus overlooking the long-term physicochemical changes that MPs undergo once they are trapped in tissues. In this study, we observed pronounced alterations in the surface properties of polystyrene MPs after one year of exposure to artificial body fluids, including increased surface roughness and hydrophilicity. These changes enhanced the adhesion of biomolecules, such as lipopolysaccharide (LPS), a typical pathogen-associated molecular pattern (PAMP). Biomechanical analysis confirmed strong interactions between aged MPs and LPS. Once phagocytosed by macrophages, LPS-loaded aged MPs caused phagolysosomal damage and pyroptosis through noncanonical caspase-11 inflammasome activation, which in turn amplified canonical caspase-1-dependent inflammation. Importantly, the inflammatory impact of aged MPs was further validated in vivo in a dextran sulfate sodium (DSS)-induced colitis model in which aged MPs aggravated disease severity. Collectively, these results identify aged MPs as "Trojan horses" with enhanced ability to transport harmful extracellular biomolecules like LPS into the cytoplasm, thereby reprogramming inflammasome signaling. This study highlights particulate stimuli, such as aged MPs, as a previously unrecognized bridge-linking PAMPs with danger-associated molecular patterns (DAMPs).
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Video S2. Interaction between aged MPs and LP
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After one year in artificial body fluids, polystyrene microplastics showed increased surface roughness and hydrophilicity that enhanced adhesion of lipopolysaccharide, a bacterial toxin. When phagocytosed by macrophages, these aged microplastic-LPS complexes triggered inflammasome activation and pyroptosis, and worsened colitis severity in mice, identifying aged microplastics as 'Trojan horses' for amplifying inflammatory responses.
Video S6: Trojan Horse Effect of Biologically Aged Microplastics-An Intracellular Carrier of LPS for Licensing Noncanonical Inflammasome Activation
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This video supplemental documents forces applied to LPS molecules bound to the surface of biologically aged microplastics along the z-axis, accompanying research on the Trojan Horse effect of aged microplastics as intracellular LPS carriers that activate noncanonical inflammasome pathways. The data supports mechanistic understanding of how weathered microplastics potentiate inflammatory immune responses.
Supporting information file for: Trojan Horse Effect of Biologically Aged Microplastics-An Intracellular Carrier of LPS for Licensing Noncanonical Inflammasome Activation
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Supporting data for a Trojan horse study showed that biologically aged microplastics—which accumulate a protein corona and adsorb lipopolysaccharide (LPS)—activate the noncanonical NLRP3/caspase-11 inflammasome pathway intracellularly, exacerbating intestinal inflammation in colitis models. This is highly significant to microplastic health research as it demonstrates that environmental aging transforms microplastics into active intracellular carriers of bacterial toxins, amplifying immune pathology beyond the particle effect alone.
Sterile inflammation induced by respirable micro and nano polystyrene particles in the pathogenesis of pulmonary diseases
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Researchers exposed human lung and immune cells to polystyrene micro and nanoparticles and found they triggered a type of inflammation that does not require infection, called sterile inflammation. Aged (oxidized) particles and those that interacted with immune cells were especially potent at activating inflammatory pathways including the NLRP3 inflammasome. This suggests that breathing in airborne microplastics could cause chronic lung inflammation over time.
Polystyrene microplastics induce an immunometabolic active state in macrophages
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Researchers found that polystyrene microplastics taken up by macrophages — immune cells lining the gut and lungs — triggered a metabolic shift toward an inflammatory state. This finding suggests microplastics reaching human tissues may alter immune function in ways that could contribute to inflammation-related diseases.
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