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Environmental influences on macrophage epigenetics and trained immunity: a review
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This review pulls together existing research showing that everyday exposures—like pollution, pesticides, certain chemicals, diet, and even stress—can leave lasting marks on immune cells called macrophages, essentially "training" them to overreact or underreact long after the initial exposure is gone. This matters because it suggests our environment may be quietly reprogramming our immune system in ways linked to chronic disease, though scientists still don't know much about newer concerns like microplastics or whether these changes can be passed to future generations. The takeaway: what we're exposed to may shape our immune health for years, making this an important area for future research and public health policy.
Macrophages are central to host immunity and tissue homeostasis, exhibiting remarkable functional plasticity across a continuum of states-ranging from pro-inflammatory (M1-like) to anti-inflammatory and tissue-reparative (M2-like) phenotypes. Environmental exposures can induce persistent epigenetic changes that shape macrophage responses well beyond the acute phase, a phenomenon now recognized as trained immunity. This narrative review synthesizes current knowledge on how diverse components of the exposome-including diet, air pollution, agricultural chemicals, heavy metals, endocrine-disrupting chemicals, per- and polyfluoroalkyl substances (PFAS), alcohol, smoking, the gut microbiome, maternal diet, and psychosocial stress-remodel the macrophage epigenome. We examine the underlying epigenetic mechanisms, namely DNA methylation, histone modifications, and non-coding RNAs, and discuss their impact on macrophage polarization, cytokine production, and trained immunity induction. Special emphasis is placed on the distinction between bona fide trained immunity and transient inflammatory skewing, the limitations of the classical M1/M2 framework, and the identification of "epigenetic vulnerability nodes" at which multiple environmental signals converge on a small set of chromatin-modifying enzymes and transcription factors. We also highlight critical knowledge gaps, including the lack of data for emerging contaminants such as micro- and nanoplastics, the uncertain reversibility of exposure-induced epigenetic marks, and the challenge of demonstrating transgenerational inheritance in humans. By connecting molecular mechanisms with broader public health implications, this review provides a critical framework for understanding environmentally driven immune dysregulation and outlines future research directions, including mixture toxicology, single-cell multi-omics, and the integration of epigenetic endpoints into chemical risk assessment.
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Western lifestyle linked to maladaptive trained immunity
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This review examines how aspects of Western lifestyle, including diet, chronic stress, and environmental exposures to air pollution and microplastics, may trigger maladaptive trained immunity in innate immune cells. Trained immunity normally provides a survival advantage by making immune cells more responsive after an initial stimulus, but chronic activation can exacerbate inflammatory diseases. The authors suggest that microplastics and other modern environmental triggers may contribute to persistent, harmful immune reprogramming.
Environmental bisphenol A exposure triggers trained immunity-related pathways in monocytes
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Researchers discovered that environmental exposure to bisphenol A, a chemical commonly found in plastics, can trigger a process called trained immunity in human immune cells from healthy individuals. This means that even after the chemical is removed, the immune cells remain in a heightened state of activation, which could contribute to chronic inflammation. The study is among the first to show that a plastic-derived compound can reprogram the immune system in this lasting way.
Immune–Epigenetic Effects of Environmental Pollutants: Mechanisms, Biomarkers, and Transgenerational Impact
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This review examines how environmental pollutants, including microplastics, heavy metals, and endocrine-disrupting chemicals, can alter immune function through epigenetic changes that modify gene expression without changing DNA itself. Researchers identified common molecular pathways through which these pollutants trigger inflammation and immune disruption. The study also highlights evidence that some of these epigenetic changes may be passed to future generations.
Micro- and Nanoplastics and the Immune System: Mechanistic Insights and Future Directions
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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.
The Emerging Threat of Micro- and Nanoplastics on the Maturation and Activity of Immune Cells
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This review examines how micro and nanoplastics affect the immune system, focusing on their impact on immune cell development and function. Studies show that these tiny plastic particles can alter how immune cells mature and respond to threats, potentially weakening the body's defenses or triggering excessive inflammation. Since humans are constantly exposed to microplastics through food, water, and air, understanding these immune effects is critical for assessing long-term health risks.
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