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Effect of micro- and nanoplastics as food contaminants on the immune system
Summary
This review synthesized research on how microplastic and nanoplastic exposure affects immune system function, finding evidence across multiple studies that these particles can modulate immune responses and trigger inflammatory pathways in exposed organisms. The authors highlight immune disruption as an emerging health concern from micro- and nanoplastic contamination.
Currently, due to the increase in the distribution and accumulation of microplastics and nanoplastics (MP and NP) in the environment, their negative impact on human health has become a global problem. The purpose of this research was to analyze the results of the studies on the effect of MPs and NPs on the body and evaluate their impact as pathogenetic factors of immune status disorders in vitro and in vivo. Material and methods. The search for literary sources was carried out in the PubMed Internet resource, and the Scopus and Web of Science databases were also used. The Springer and Elsevier websites were used to access the full text of the articles. Results. MP and NP enter the human body through ingestion of food, water, as well as through inhalation and contact with the skin. The results of the studies indicate that MP and NP particles, entering the human body, can move along with the blood and accumulate in various organs: the liver, spleen, heart, lungs, thymus, reproductive organs, kidneys and brain, i.e., to overcome the blood-brain barrier. The immune system is the main regulatory and protective system of the body, playing a major role in the recognition and destruction of foreign antigens of a viral, bacterial and chemical nature. Innate immunity is the first line of defense against pathogens. Macrophages, monocytes, natural killer cells (NK cells), and leukocytes (neutrophils) phagocytize antigens and present them to adaptive immune cells. It has been established that the damaging effect of MPs and NPs on immunity (immunotoxicity) is mainly due to the presence of oxidative stress with the formation of reactive oxygen species (ROS) and damage-associated molecular patterns (DAMP). The toxicity of MPs and NPs is realized by reducing the expression of the Nrf2 factor (a redox-sensitive transcription factor that regulates antioxidant protection) and the activation of p38 mitogen-activated protein kinases. In addition, it was found that the inflammatory process after exposure to MP and NPs is mediated by the expression of pro-inflammatory cytokines: IFN-γ, TNF-α, IL-1β, IL-6 and IL-33 and a decrease in the expression of cytokines: IL-4, IL-5, IL-10, IL-33 and TGF-β1, which leads to activation of the signal transducer and activator of transcription 3 (STAT3), nuclear factor kappa B (NF-κB) and cGas/STING pathways. Conclusion. Analysis of the data of MP and NP effect on the immune system indicates the presence of aseptic chronic inflammation, which requires studying the causes and mechanisms of the development of inflammatory processes.
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