Asset Details
Do you wish to reserve the book?
PVC Nanoplastics Exposure Exacerbates Asthma through R‐Loop Accumulation and Subsequent STING Activation in Macrophages
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
PVC Nanoplastics Exposure Exacerbates Asthma through R‐Loop Accumulation and Subsequent STING Activation in Macrophages
Do you wish to request the book?
PVC Nanoplastics Exposure Exacerbates Asthma through R‐Loop Accumulation and Subsequent STING Activation in Macrophages
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
PVC Nanoplastics Exposure Exacerbates Asthma through R‐Loop Accumulation and Subsequent STING Activation in Macrophages
2025
Overview
Asthma is a chronic inflammatory respiratory disease influenced by genetic and environmental factors. Emerging evidence suggests that microplastics and nanoplastics (NPs) pose significant health risks. When inhaled, these tiny particles can accumulate in the lungs, triggering inflammation, oxidative stress, and other disruptions in pulmonary function. This study investigates the role of polyvinyl chloride (PVC) NPs, which are extensively used in products such as packaging, medical devices, and construction materials, in asthma pathogenesis. Using an ovalbumin (OVA)‐induced murine asthma model, it is demonstrated that PVC NPs exposure exacerbates airway hyperresponsiveness, increases inflammatory cell infiltration, and elevates inflammatory cytokine levels in the lungs. Further mechanistic studies reveal that PVC NPs suppress Ribonuclease H1 (RNASEH1), leading to RNA–DNA hybrid loop (R‐loop) accumulation and activation of the Cyclic GMP‐AMP Synthase (cGAS)‐Stimulator of Interferon Genes (STING) inflammatory pathway. The critical involvement of this pathway is confirmed using STING‐deficient mice, where pathway inhibition alleviates the inflammation exacerbated by PVC NPs exposure. These findings provide new insights into the potential role of NPs pollutants in modulating immune responses through R‐loop formation, linking PVC NPs to asthma pathogenesis. This study highlights the importance of addressing environmental exposure to NPs in asthma prevention and management and identifies potential molecular targets for therapeutic intervention. Polyvinyl chloride (PVC) nanoplastics (NPs) are shown to aggravate allergic airway inflammation in asthma by triggering R‐loop accumulation and activating the cGAS‐STING pathway in macrophages. This study reveals a novel immunotoxic mechanism linking environmental plastic exposure to asthma pathogenesis and highlights potential molecular targets for mitigating nanoplastic‐induced respiratory inflammation.
Publisher
John Wiley & Sons, Inc,Wiley
