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Urban Air, Diesel Exhaust and Microplastic Particles Predispose to Asthma Origin Via Gut Microbiome Alteration
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Researchers found that prenatal exposure of mice to urban air particles, diesel exhaust, or microplastic particles predisposed newborns to developing asthma through alterations in gut microbiome composition. By transplanting gut flora from exposed pups to unexposed recipients, they confirmed that the altered microbiome alone was sufficient to trigger asthma susceptibility. The study suggests that airborne particle exposure may contribute to asthma development via gut microbiome disruption rather than direct lung effects.
Abstract Rationale. Emerging findings link asthma and allergy to gut microbiome alterations, however causality remains largely unproven. Asthma onset can be promoted by environmental airborne particles, but mechanisms are poorly understood. At the same time, pulmonary particle exposure was shown to alter gut microbiome. Among the particles microplastics are a ‘new’ type and are increasingly found in the organism of humans; accumulating evidence implies health risks, but often no link to disease is seen making causality hard to establish. Our mouse model integrates these factors for a mechanistic study of asthma origin: prenatal exposure to environmental particles concentrated from urban air (CAP), diesel exhaust particles (DEP) or microplastic particles (MP) predisposes neonates to asthma. We hypothesized that particle-altered gut flora mediates asthma predisposition, and aimed to identify causative microbiome components and their metabolic activity operative in modulating immune signaling. Methods. Airway exposure of pregnant dams to CAP, DEP or MP triggers predisposition to asthma in newborns, so that they develop asthma after an intentionally low-dose of allergen that is innocuous in control pups. Here we performed gut microbiome transplant (GMT) from these asthma-predisposed neonates (without any allergen exposure) to intact recipients: asthma onset was determined as airway hyperresponsiveness, eosinophilia in bronchoalveolar lavage, lung tissue infiltration and elevation of IL-4, IL-5 and IL-13. Microbiome and metabolite changes were tested by metagenomic sequencing and metabolomics. Results. GMT conferred asthma predisposition to naïve recipients in all three particle groups. To test whether live microbes are required for the effect we radiation sterilized the GMT material, which ablated its ability to confer disease. To narrow down the effect we co-treated the GMT with antibacterials which also abrogated the GMT effect. Metagenomics revealed that more abundant in the CAP and DEP samples were Acetatifactor, Butyribacter, Kineothrix, Coproplasma and Lachnospiraceae bacteria (MP samples are work-in-progress). Functional analysis suggested a potential mechanistic explanation: these ‘suspect’ species are linked to short-chain fatty acids (acetate, butyrate) production known to affect dendritic cells (DCs). When tested, we found acetate and butyrate levels altered and DC function skewed toward allergy responses. Conclusions. Prenatal exposure to CAP, DEP or MP particles changes the gut microbiome of newborns making it causative of increased asthma predisposition. Live, but not dead, microbiome transplant confers the effect to recipients. Metagenomics identified potential bacteria ‘suspects’, informing future species-specific studies. The microbiome interaction with host immunity involves bacteria-derived fatty acids that modulate DC function leading to enhanced allergen presentation.
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