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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.
SEM, EDS, py-GCMS, surface functional group analysis, characterization of MPs, surface roughness analysis, protein adsorption and LPS, binding and binding force of pristine and aged microplastics to LPS, caspase-11-dependent sensing progression of colitis, gating strategies, Rhodamine 123 loading, and densitometric quantification
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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.
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.
Relationship Between Particle Properties and Immunotoxicological Effects of Environmentally-Sourced Microplastics
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Researchers exposed human macrophages to environmentally collected and weathered microplastic particles from the North Pacific Gyre and French coast to assess immunotoxicity, finding that particle physicochemical properties including polymer type and surface chemistry correlated with different cytokine response profiles. Multi-dimensional analysis revealed that surface area and hydrophobicity were key predictors of macrophage immune activation.
Multiomics RevealsNonphagocytosable MicroplasticsInduce Colon Inflammatory Injury via Bile Acid-Gut Microbiota Interactionsand Barrier Dysfunction
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Mice were given long-term oral exposure to 10 µm polystyrene microplastics (too large for cellular uptake) and colonic inflammatory injury was assessed using multi-omics. Non-phagocytosable microplastics disrupted the colonic redox balance, elevated the Th17/Treg ratio, and caused colitis through bile acid-gut microbiota interactions and intestinal barrier dysfunction.
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