Polystyrene Nanoplastics Drive β‐Cell Dedifferentiation Through Dendritic Cell‐Intrinsic MHC‐I‐Dependent Inflammatory Crosstalk
5 affiliations
- 1Key Laboratory of Precision Nutrition and Health Ministry of Education Department of Nutrition and Food Hygiene the National Key Discipline School of Public Health Harbin Medical University Harbin People's Republic of China
- 2Department of Neurology The First Affiliated Hospital of Anhui Medical University Anhui Medical University Hefei People's Republic of China
- 3Department of Toxicology College of Public Health Harbin Medical University Harbin Heilongjiang People's Republic of China
- 4Department of Vascular Surgery Beijing Friendship Hospital Capital Medical University Beijing People's Republic of China
- 5Department of Cardiology the First Affiliated Hospital of Harbin Medical University Harbin People's Republic of China
Abstract
Environmental nanoplastic exposure is linked to metabolic disorders, yet its impact on pancreatic immune‐endocrine homeostasis and β‐cell identity regulation remains poorly defined. Rats were exposed to polystyrene nanoplastics(PS‐NPs) for 12 weeks under a control or high‐fat diet. Pancreatic injury and phenotypes were assessed biochemically, histologically, and ultrastructurally; single‐nucleus RNA‐seq delineated cell‐specific transcription and intercellular networks. Mechanistic validation used cell co‐cultures with MHC‐I modulation, and translational relevance was assessed in a human exposure cohort. Chronic PS‐NPs exposure exacerbated hyperglycemia and glucose intolerance, and induced pancreatic damage. Single‐nucleus transcriptomics identified β cells and dendritic cells (DCs) as the most responsive populations. PS‐NPs drove β‐cell dedifferentiation, characterized by downregulation of key identity markers (Mafa, Pdx1, Nkx6.1). Concurrently, DCs exhibited a maturation‐like phenotype with robust upregulation of MHC‐I and inflammatory pathways. Ligand‐receptor analysis revealed enhanced proinflammatory crosstalk between DCs and β cells. Functionally, MHC‐I upregulation in DCs activated TLR4/NF‐κB signaling and drove β‐cell dedifferentiation in vitro. Consistently, occupationally exposed individuals showed elevated circulating HLA‐A levels and metabolic abnormalities. These findings identify an MHC‐I‐dependent DCs‐β‐cell inflammatory axis through which PS‐NPs disrupt pancreatic immune‐endocrine homeostasis and promote β‐cell dedifferentiation, revealing mechanisms underlying PS‐NPs‐induced metabolic dysfunction.
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BibTeX
@article{qiao2026polystyrene,
title = {{Polystyrene Nanoplastics Drive β‐Cell Dedifferentiation Through Dendritic Cell‐Intrinsic MHC‐I‐Dependent Inflammatory Crosstalk}},
author = {Conghui Qiao and Yuqing Song and Fang Yang and Menghui Guo and Libin Jiang and Xiaoyue Quan and Wei Wei and Xinyang Wang and Tianshu Han and Mingyuan Liu and Wenbo Jiang},
journal = {Advanced Science},
year = {2026},
month = aug,
doi = {10.1002/advs.77096},
url = {https://doi.org/10.1002/advs.77096},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Polystyrene Nanoplastics Drive β‐Cell Dedifferentiation Through Dendritic Cell‐Intrinsic MHC‐I‐Dependent Inflammatory Crosstalk
AU - Conghui Qiao
AU - Yuqing Song
AU - Fang Yang
AU - Menghui Guo
AU - Libin Jiang
AU - Xiaoyue Quan
AU - Wei Wei
AU - Xinyang Wang
AU - Tianshu Han
AU - Mingyuan Liu
AU - Wenbo Jiang
PY - 2026
DA - 2026/08/17
JO - Advanced Science
DO - 10.1002/advs.77096
UR - https://doi.org/10.1002/advs.77096
AB - Environmental nanoplastic exposure is linked to metabolic disorders, yet its impact on pancreatic immune‐endocrine homeostasis and β‐cell identity regulation remains poorly defined. Rats were exposed to polystyrene nanoplastics(PS‐NPs) for 12 weeks under a control or high‐fat diet. Pancreatic injury and phenotypes were assessed biochemically, histologically, and ultrastructurally; single‐nucleus RNA‐seq delineated cell‐specific transcription and intercellular networks. Mechanistic validation used cell co‐cultures with MHC‐I modulation, and translational relevance was assessed in a human exposure cohort. Chronic PS‐NPs exposure exacerbated hyperglycemia and glucose intolerance, and induced pancreatic damage. Single‐nucleus transcriptomics identified β cells and dendritic cells (DCs) as the most responsive populations. PS‐NPs drove β‐cell dedifferentiation, characterized by downregulation of key identity markers (Mafa, Pdx1, Nkx6.1). Concurrently, DCs exhibited a maturation‐like phenotype with robust upregulation of MHC‐I and inflammatory pathways. Ligand‐receptor analysis revealed enhanced proinflammatory crosstalk between DCs and β cells. Functionally, MHC‐I upregulation in DCs activated TLR4/NF‐κB signaling and drove β‐cell dedifferentiation in vitro. Consistently, occupationally exposed individuals showed elevated circulating HLA‐A levels and metabolic abnormalities. These findings identify an MHC‐I‐dependent DCs‐β‐cell inflammatory axis through which PS‐NPs disrupt pancreatic immune‐endocrine homeostasis and promote β‐cell dedifferentiation, revealing mechanisms underlying PS‐NPs‐induced metabolic dysfunction.
SN - 2198-3844
ER -