We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Micro- and Nanoplastics and the Immune System: Mechanistic Insights and Future Directions
Summary
This review summarizes how micro- and nanoplastics disrupt the human immune system at the cellular level, impairing key immune cells like macrophages, dendritic cells, and T cells. The particles trigger chronic low-grade inflammation through oxidative stress and activation of inflammatory pathways, and can worsen autoimmune conditions like lupus and inflammatory bowel disease in animal studies. These findings raise concerns that ongoing microplastic exposure could gradually weaken immune function and contribute to immune-related diseases in people.
Micro- and nanoplastics (MNPs) are emerging environmental immunotoxins with widespread human exposure through ingestion, inhalation, and dermal contact. Detected in the placenta, lungs, blood, bone marrow, and brain, MNPs accumulate in immune organs where they disrupt innate and adaptive cell functions. This review aims to provide a comprehensive summary of the current knowledge on how MNPs affect the immune system at the cellular and molecular levels. Experimental evidence shows that MNPs impair macrophage phagocytosis, skew dendritic cell maturation, trigger neutrophil extracellular traps, and alter T and B cell responses. Mechanistically, these effects are driven by oxidative stress, mitochondrial dysfunction, and activation of key inflammatory signaling pathways, including NF-κB, MAPK, and NLRP3 inflammasome, leading to apoptosis, pyroptosis, and chronic low-grade inflammation. Furthermore, MNP-induced disruption of epithelial barriers and gut microbiota composition undermines immune tolerance and contributes to the pathogenesis of autoimmune conditions. Preclinical models provide evidence linking MNP exposure to exacerbation of diseases such as systemic lupus erythematosus, inflammatory bowel disease, and rheumatoid arthritis. However, human epidemiological data remain limited, highlighting the urgent need for standardized exposure protocols, advanced omics technologies, and longitudinal cohort studies are urgently needed to establish causal links and inform public health strategies.