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Unraveling the impact of microplastics on autoimmune diseases: hidden dangers and environmental triggers
Summary
This review examines the emerging evidence linking microplastic exposure to the development and progression of autoimmune disorders. Researchers found that microplastics can modulate immune gene expression, trigger excessive reactive oxygen species in immune cells, and promote inflammatory cytokine release, potentially creating conditions favorable for autoantibody production. The study highlights microplastics as a plausible environmental trigger for autoimmune conditions, though direct causal evidence in humans remains limited.
Autoimmune diseases (ADs) are a heterogeneous group of disorders characterized by loss of immune tolerance against self-antigens, leading to local or systemic inflammation and subsequent tissue/organ damage. Until now, the etiology of ADs remains obscure. Growing evidence suggests that microplastics (MPs) may act as emerging environmental triggers in the initiation and progression of these disorders. MPs have been shown to modulate immune-related gene expression and induce excessive reactive oxygen species production in various immune cells, such as macrophages, T cells, and B cells. This may lead to the release of pro-inflammatory cytokines and could create conditions that may promote the production of autoantibodies. Moreover, MPs can activate neutrophils and natural killer cells, potentially exacerbating immune dysregulation and chronic inflammation. Additionally, plasticizers and other chemical additives in MPs interact with immune cells via nuclear and membrane receptors, suggested to cause mitochondrial dysfunction and potentially further compromise immune homeostasis. Given the increasing presence of MPs in the environment and their potential immunomodulatory effects, understanding their role in ADs is of critical importance. This review summarizes the recent evidence and unveils the potential impact of MPs on immune functions and the pathogenesis of major ADs, including systemic lupus erythematosus, rheumatoid arthritis, and inflammatory bowel disease. Furthermore, we highlight future research directions to better understand the influences of MPs on ADs.
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