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Inflammatory Microenvironment Reshapes the Protein Corona of Polystyrene Nanoplastics to Exacerbate Periodontitis Progression
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This research explored valorization strategies for marine-sourced polypropylene waste, converting recovered PP plastic into useful materials or chemicals through mechanical, thermal, or chemical recycling. The study demonstrates that marine plastic debris can serve as a feedstock for value-added product creation, supporting marine cleanup incentives.
Nanoplastics (NPs) are emerging environmental pollutants with widespread human exposure and potential health risks. Once entering biological systems, NPs readily acquire a protein corona (PC) that governs their biological identity and toxicity. However, how disease-associated microenvironments reshape PC and modulate NPs toxicity remains poorly understood. Here, we investigated the effects of the oral inflammatory microenvironment on PC and the biological behavior of polystyrene (PS) NPs using periodontitis as a model disease. We identified a disease-specific PC formed in the saliva of periodontitis patients, characterized by enrichment of apolipoproteins, complement, and coagulation proteins. Compared with the normal PC, this disease-specific PC markedly enhanced macrophage uptake of PS NPs via increased phagocytosis and lipid raft/caveolin-mediated endocytosis, and triggered stronger pro-inflammatory responses, including elevated reactive oxygen species production, M1 macrophage polarization, and cytokine secretion. In vivo, oral exposure to PS NPs exacerbated alveolar bone loss and inflammation in a periodontitis mouse, accompanied by enhanced macrophage M1 polarization and systemic inflammatory responses. Mechanistically, these effects were closely associated with the complement-enriched disease-specific PC that amplified NPs-immune cell interactions. Overall, this study demonstrates that inflammatory microenvironments can reshape the PC of NPs and intensify their toxicological outcomes, underscoring the need for health-dependent risk assessment of NPs.
More Papers Like This
Inflammatory Microenvironment Reshapes the Protein Corona of Polystyrene Nanoplastics to Exacerbate Periodontitis Progression (Adv. Healthcare Mater. 22/2026)
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Tiny plastic particles (nanoplastics) that end up in your mouth don't act the same way in healthy gums as they do in gums already inflamed by gum disease — when inflammation is present, these particles pick up a different coating of proteins that makes them more likely to trigger immune cells and worsen tissue damage. This "vicious cycle" effect suggests that people with existing gum disease may be more vulnerable to harm from environmental nanoplastic exposure, highlighting a new health risk worth watching as plastic pollution continues to build up in our bodies.
Periodontal Disease, Chronic Silent Inflammation, and Micro/Nanoplastics: An Environmental Microbiology Review of Oral Biofilm Retention, Dysbiosis, and Systemic Risk Pathways
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This research developed cassava starch-based bioplastics, evaluating the mechanical, thermal, and biodegradation properties of starch-composite materials as alternatives to conventional petroleum-derived plastics. The study demonstrates that cassava starch can serve as a viable raw material for biodegradable packaging applications in tropical regions.
The in vitro gastrointestinal digestion-associated protein corona of polystyrene nano- and microplastics increases their uptake by human THP-1-derived macrophages
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When polystyrene nano- and microplastics pass through simulated gastrointestinal digestion, they acquire a coating of gut proteins — a 'protein corona' — that dramatically increases their uptake by human immune cells (macrophages), boosting internalization of small neutral particles by up to six-fold compared to undigested plastic. The identity of the proteins driving this effect, including clotting factors and apolipoproteins, suggests that realistic dietary exposure conditions substantially change how microplastics interact with the body, and that lab tests using undigested plastics likely underestimate actual cellular uptake.
Micro/Nanoplastics and Periodontitis: An Environmental Microbiology Perspective on Oral Retention and Systemic Risk
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Researchers reviewed evidence through a three-tier evidentiary framework and found that human dental calculus harbors at least 26 microplastic types — dominated by polyamide and polyethylene — where polyethylene induces cytotoxicity and NF-κB-driven inflammation in gingival fibroblasts, suggesting the periodontal pocket may act as a particle-retention niche that amplifies systemic inflammatory risk.
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.
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