tetano
Editor, Senior Moderator
Front Immunol
. 2024 May 13:15:1382655.
doi: 10.3389/fimmu.2024.1382655. eCollection 2024. Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung
Cameron R Bishop[SUP] 1 [/SUP], Kexin Yan[SUP] 1 [/SUP], Wilson Nguyen[SUP] 1 [/SUP], Daniel J Rawle[SUP] 1 [/SUP], Bing Tang[SUP] 1 [/SUP], Thibaut Larcher[SUP] 2 [/SUP], Andreas Suhrbier[SUP] 1 3 [/SUP]
Affiliations
Introduction: Global microplastic (MP) pollution is now well recognized, with humans and animals consuming and inhaling MPs on a daily basis, with a growing body of concern surrounding the potential impacts on human health.
Methods: Using a mouse model of mild COVID-19, we describe herein the effects of azide-free 1 μm polystyrene MP beads, co-delivered into lungs with a SARS-CoV-2 omicron BA.5 inoculum. The effect of MPs on the host response to SARS-CoV-2 infection was analysed using histopathology and RNA-Seq at 2 and 6 days post-infection (dpi).
Results: Although infection reduced clearance of MPs from the lung, virus titres and viral RNA levels were not significantly affected by MPs, and overt MP-associated clinical or histopathological changes were not observed. However, RNA-Seq of infected lungs revealed that MP exposure suppressed innate immune responses at 2 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 observed in some COVID-19 patients.
Discussion: The findings are consistent with the recent finding that MPs can inhibit phagocytosis of apoptotic cells via binding of Tim4. They also add to a growing body of literature suggesting that MPs can dysregulate inflammatory processes in specific disease settings.
Keywords: COVID-19; RNA-Seq; SARS-CoV-2; inflammation; microplastics; mouse.
. 2024 May 13:15:1382655.
doi: 10.3389/fimmu.2024.1382655. eCollection 2024. Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung
Cameron R Bishop[SUP] 1 [/SUP], Kexin Yan[SUP] 1 [/SUP], Wilson Nguyen[SUP] 1 [/SUP], Daniel J Rawle[SUP] 1 [/SUP], Bing Tang[SUP] 1 [/SUP], Thibaut Larcher[SUP] 2 [/SUP], Andreas Suhrbier[SUP] 1 3 [/SUP]
Affiliations
- PMID: 38803494
- PMCID: PMC11128561
- DOI: 10.3389/fimmu.2024.1382655
Introduction: Global microplastic (MP) pollution is now well recognized, with humans and animals consuming and inhaling MPs on a daily basis, with a growing body of concern surrounding the potential impacts on human health.
Methods: Using a mouse model of mild COVID-19, we describe herein the effects of azide-free 1 μm polystyrene MP beads, co-delivered into lungs with a SARS-CoV-2 omicron BA.5 inoculum. The effect of MPs on the host response to SARS-CoV-2 infection was analysed using histopathology and RNA-Seq at 2 and 6 days post-infection (dpi).
Results: Although infection reduced clearance of MPs from the lung, virus titres and viral RNA levels were not significantly affected by MPs, and overt MP-associated clinical or histopathological changes were not observed. However, RNA-Seq of infected lungs revealed that MP exposure suppressed innate immune responses at 2 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 observed in some COVID-19 patients.
Discussion: The findings are consistent with the recent finding that MPs can inhibit phagocytosis of apoptotic cells via binding of Tim4. They also add to a growing body of literature suggesting that MPs can dysregulate inflammatory processes in specific disease settings.
Keywords: COVID-19; RNA-Seq; SARS-CoV-2; inflammation; microplastics; mouse.