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Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Marine & Wildlife Policy & Risk Sign in to save

Immune response to polystyrene microplastics: Regulation of inflammatory response via the ROS-driven NF-κB pathway in zebrafish (Danio rerio)

Aquatic Toxicology 2025 9 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 63 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Jincheng Pei, Jincheng Pei, Jincheng Pei, Jincheng Pei, Shannan Chen, Shannan Chen, Q Ke, Q Ke, Anning Pang, Anning Pang, Anning Pang, Anning Pang, Mengmeng Niu, Mengmeng Niu, Nan Li, Jiayi Li, Zhi Wang, Nan Li, Hongjuan Wu, Hongjuan Wu, Hongjuan Wu, Hongjuan Wu, Pin Nie Pin Nie

Summary

Researchers found that polystyrene microplastics triggered immune system inflammation in zebrafish by generating reactive oxygen species (ROS) that activated the NF-kB signaling pathway. The microplastics accumulated mainly in the intestines, causing tissue damage and behavioral changes in the fish. This study identifies a specific molecular mechanism by which microplastics cause immune dysfunction, which could be relevant to understanding inflammation in humans exposed to microplastics.

Polymers

There is increasing apprehension regarding the rising prevalence of microplastics (MPs) in aquatic ecosystems. Although MPs cause toxicological effect on fish via diverse pathways, the precise immunotoxicological mechanism is yet to be fully understood. Utilizing zebrafish in early developmental stages and zebrafish embryonic fibroblast (ZF4) as models, this study delved into the immune response elicited by polystyrene MPs (PS-MPs). It was observed that larvae predominantly accumulate 3 μm PS-MPs in their intestines through ingestion, leading to notable changes in locomotor behavior and histopathological alterations. Further investigation revealed that short-term exposure to PS-MPs triggers oxidative stress (OS) and inflammation in zebrafish. This is evidenced by the upregulation of OS and inflammation-related genes, increased levels of reactive oxygen species (ROS), malonaldehyde (MDA), and inflammatory cytokines, altered activities of antioxidant enzymes, along with induced recruitment of leukocyte in larvae. Cellular assays confirmed that PS-MPs elevate intracellular ROS in ZF4 cells and enhance the nuclear translocation of NF-κB P65. Notably, the activation of NF-κB and the upsurge in inflammatory cytokines can be mitigated by inhibiting ROS. This research highlights the significance of the ROS-triggered NF-κB signaling cascade in PS-MPs-mediated inflammation within zebrafish, illuminating the possible processes that underlie the innate immune system of fish toxicity caused by MPs.

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