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Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung
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Using a mouse model of mild COVID-19, this study found that microplastic beads co-delivered to the lungs alongside SARS-CoV-2 suppressed early innate immune responses and later amplified pro-inflammatory signals resembling the cytokine release syndrome seen in severe COVID-19 cases. Viral load itself was unchanged, suggesting microplastics do not accelerate infection but instead disrupt the body's ability to regulate inflammation during disease. This raises concern that widespread microplastic inhalation could worsen outcomes during respiratory infections in people already carrying a lung burden of plastic particles.
ABSTRACT Global microplastic (MP) pollution is now well recognized, with humans and animals consuming and inhaling MPs on a daily basis. Herein we described the effects of azide-free, 1 µm polystyrene MP beads co-delivered into lungs with a SARS-CoV-2 omicron BA.5 inoculum using a mouse model of mild COVID-19. Lung virus titres and viral RNA levels were not significantly affected by MPs, with overt clinical or histopathological changes also not observed. However, RNA-Seq of infected lungs revealed that MP exposure suppressed innate immune responses at 2 days post infection (dpi) and increased pro-inflammatory signatures at 6 dpi. The cytokine profile at 6 dpi showed a significant correlation with the ‘cytokine release syndrome’ signature seen in some severe COVID-19 patients. This study adds to a growing body of literature suggesting that MPs can dysregulate inflammation in specific disease settings. Graphical Abstract HIGHLIGHTS A single inoculation of microplastics dysregulated SARS-CoV-2 lung inflammation At the peak of SARS-CoV-2 infection microplastics decreased early innate responses Later post infection microplastics promoted a “cytokine release syndrome” signature A key mechanism may involve the inhibition of the phagocytosis of infected cells Azide-free microplastics were used, with no elevated ROS responses identified Postulated mechanisms whereby microplastics might decrease the proinflammatory responses 2 days after SARS-CoV-2 infection, yet promote the proinflammatory ‘cytokine release syndrome’ signature at 6 days post infection.
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