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Mitigating microplastic-induced organ Damage: Mechanistic insights from the microplastic-macrophage axes
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This review is the first comprehensive examination of how microplastics interact with macrophages, the immune cells responsible for engulfing and removing foreign particles from the body. When macrophages absorb microplastics, the resulting oxidative stress disrupts their normal function, leading to inflammation and organ damage, with gut bacteria potentially playing a role in this harmful process.
We live in a world increasingly dominated by plastic, leading to the generation of microplastic particles that pose significant global health concerns. Microplastics can enter the body via ingestion, inhalation, and direct contact, accumulating in various tissues and potentially causing harm. Despite this, the specific cellular mechanisms and signaling pathways involved remain poorly understood. Macrophages are essential in absorbing, distributing, and eliminating microplastics, playing a key role in the body's defense mechanisms. Recent evidence highlights oxidative stress signaling as a key pathway in microplastic-induced macrophage dysfunction. The accumulation of microplastics generates reactive oxygen species (ROS), disrupting normal macrophage functions and exacerbating inflammation and organ damage. This review serves as the first comprehensive examination of the interplay between microplastics, macrophages, and oxidative stress. It discusses how oxidative stress mediates macrophage responses to microplastics and explores the interactions with gut microbiota. Additionally, it reviews the organ damage resulting from alterations in macrophage function mediated by microplastics and offers a novel perspective on the defense, assessment, and treatment of microplastic-induced harm from the viewpoint of macrophages.
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Impact of microplastics on human health: A critical role of gut microbiota
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Researchers systematically reviewed how microplastics traverse biological barriers and deposit in human organs, documenting that ingested MPs mechanically damage the intestinal lining, shift gut microbiota toward a Firmicutes-dominant profile, and disrupt metabolite production — changes that propagate via gut-liver and gut-brain axes to contribute to metabolic, cardiovascular, neurological, and reproductive disorders, positioning microbiome modulation as a potential therapeutic strategy.
The ant that may well destroy a whole dam: a systematic review of the health implication of nanoplastics/microplastics through gut microbiota
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This systematic review summarizes existing research on how nanoplastics and microplastics disrupt gut bacteria in various organisms. The findings show that plastic particle exposure consistently alters gut microbiome composition, which in turn affects the host's immune function, metabolism, and overall health. These gut bacteria changes may be a key pathway through which microplastics harm human health.
Ingestion of micro- and nanoplastic perturbs tissue homeostasis and macrophage core functions
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Researchers fed mice polystyrene particles chronically and found that micro- and nanoplastics breached intestinal barriers and accumulated in multiple organs, disrupting tissue homeostasis and impairing core macrophage functions including phagocytosis and inflammatory regulation.
Microplastic exposure and obesity-related metabolic dysfunction: A proposed gut microbiota-metabolite framework.
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This review paper summarizes existing research on how microplastics eaten with food might affect gut bacteria, gut lining health, and body fat in animal studies and lab cell experiments. It suggests microplastics could disrupt gut microbes and cause inflammation linked to obesity-related problems, but notes gaps in long-term testing and uncertainty about applying findings across species.
Microplastics as Microbiota Modulators: Rewiring the Gut Metabolism Immune Axis.
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This review summarizes existing research on how microplastics may affect gut bacteria, the gut's protective lining, and digestive chemical signals, mostly based on animal and lab cell studies. These changes were linked to inflammation and disrupted metabolism in those studies, but human evidence remains limited, and researchers call for more standardized studies.
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