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Microplastic exposure induces HSP90α secretion and aggravates asthmatic airway remodeling via PI3K-Akt-mTOR pathway
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Researchers discovered that microplastic exposure worsens asthma by damaging the airway lining and triggering the release of a stress protein called HSP90-alpha. This protein activates a signaling pathway (PI3K-Akt-mTOR) that causes airway smooth muscle cells to multiply, leading to narrower airways and increased sensitivity -- hallmarks of severe asthma. A targeted antibody that blocks HSP90 was able to reverse the lung inflammation and airway hyperresponsiveness in the study.
Microplastics pollution has raised a considerable awareness due to their extensive distribution in the environment. It has potential side effects on human health. Microplastics can enter the human respiratory system, then deposit in the lung, destroying the structure of the bronchus and alveoli, and causing pulmonary inflammation, mucus production, and airway hyperresponsiveness, leading to the aggravation of asthma. Nevertheless, the underlying mechanism remains elusive. There are several cytokines involved in the inflammatory response of asthma. Heat shock protein 90α(HSP90α) is one of cytokines involving in inflammation which is a member of the HSPs family. The aim of this study is to explore the mechanism by which microplastics influence the secretion of HSP90α and the progression of asthma. Initially, we found that microplastics were destroyed airway epithelial barrier, resulting in inherent dysfunction in the secretion of HSP90α. Then, microplastics were proved to activate PI3K-Akt-mTOR pathway by prompting airway epithelial cells secrete HSP90α and proliferation of airway smooth muscle cells(ASMCs), leading to airway narrowing and hypersensitivity. 1G6-D7 is a monoclonal antibody to HSP90, which can reverse the pulmonary inflammation infiltration, mucus production, and airway hyperresponsiveness(AHR). Overall, these finding suggested that microplastics elicited inflammation via the PI3K-Akt-mTOR signaling pathway and stimulated the proliferation of ASMCs. Hence, the present study unveils a novel mechanism responsible for microplastic-induced inflammation and airway hyperreactivity, establishing a basis for further research and risk evaluations of microplastics.
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In a mouse model of asthma, co-exposure to inhaled polyethylene microplastics and house dust mite allergens caused worse airway inflammation than either pollutant alone. The microplastics damaged the airway lining and amplified allergic reactions through a specific inflammatory signaling pathway called CXCL1. This finding suggests that breathing in airborne microplastics could make allergies and asthma worse by helping allergens penetrate deeper into the lungs.
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Researchers found tiny plastic particles (microplastics) in the lung mucus of every single child with asthma they tested, and kids with worse-controlled asthma had higher levels of these particles in their airways. Lab experiments on lung tissue models suggested these plastics may trigger harmful cell stress and inflammation, though more research is needed to confirm this actually causes the asthma symptoms rather than just being linked to them. This study is a reminder that the air we breathe, and the plastic particles in it, may be quietly affecting respiratory health, especially in children.
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This review examines how microplastics, which can enter the body through breathing, eating, and skin contact, may affect allergic airway conditions. Researchers found evidence that microplastics can damage airway lining cells, disrupt the protective barrier of the respiratory tract, and trigger heightened airway reactivity. The study suggests that chronic microplastic exposure may worsen allergic airway inflammation, though more research is needed to fully understand the mechanisms involved.
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In mice with allergic asthma triggered by house dust mites, exposure to polystyrene nanoplastics significantly worsened airway inflammation and lung damage. The nanoplastics disrupted the protective barrier of lung cells by activating a specific signaling pathway (EGFR/ERK), allowing more allergens and immune cells to penetrate lung tissue. This finding suggests that airborne nanoplastics could make asthma and allergies worse for the millions of people who already suffer from these conditions.
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