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Abstract P179: Nano- And Microplastic-enriched Diets Affect Inflammation And Target Organ Damage In Hypertension
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This study found that diets enriched with nano- and microplastics increase inflammation and worsen organ damage in rats with high blood pressure. The findings suggest that microplastic exposure may be particularly harmful for people who already have cardiovascular conditions, potentially accelerating disease progression through inflammatory pathways.
Plastic particle pollution is a major environmental challenge worldwide. Micro (MP)- and nanoplastic (NP) particles appear ubiquitously and have been detected in food, drinking water, human feces and blood. Once absorbed, plastic particles can alter the gut microbiome and induce inflammation. Current research primarily focuses on the impact on healthy organisms. Yet, a deeper understanding of the impact of MP and NP on health-to-disease transition and their impact on cardiovascular disease is missing. This project aims to investigate the impact of MP and NP in experimental hypertension. Ten-week-old male NMRI mice were randomized to receive the following particle-enriched diets: a polystyrene MP (particle size 5 μm) (20 μg/g chow, 100 μg/l via drinking water), NP (particle size 100nm) (20 μg/g chow,100 μg/l via drinking water) or control (C) for four weeks. Subsequently, hypertension (HTN) was induced by Angiotensin II (AngII) infusion (1000 ng/kg*min s.c., osmotic minipump). Sham-treated non-hypertensive mice served as controls. During hypertension induction mice were continued on their respective diets. After 14 days, we assessed hypertensive organ damage and inflammation. AngII-treated mice developed hypertension an increased cardiac hypertrophy index (Sham vs HTN: 10.1 vs 10.7 mg/mm tibia), and lower cardiac output (HTN vs Sham: 15.5 vs 19.9 ml/min, echocardiography). MP fed mice showed upregulated mRNA expression of marker genes for renal fibrosis ( Ctgf; Acta ) in both homeostasis (ddCT -2 for MP: 2.7; 6.6) and HTN (ddCT -2 3.2 (MP) vs. 2.3 (C); 14.2 (MP) vs 11.2 (C)), as well as enhanced proinflammatory gene expression ( Ccl2; IL1b ) in HTN (ddCT -2 7.4 (MP) vs 4.0 (C); 5.8 (MP) vs 4.3 (C)). Similarly, NP fed mice showed altered mRNA expression for e.g. IL1b (ddCT -2 for NP: 3.6). Flow cytometric analysis shows a proinflammatory immune response to MP and NP, e.g. an increase of circulating neutrophils (HTN C vs. MP: 24.7% vs 50.0% of CD45+) and Ly6C hi monocytes (Homeostasis C vs NP: 2.4 vs 3.2% of CD45+). Conclusion: MP and NP affect the inflammatory response and organ damage in hypertension. Our further investigations will help to shed light on the impact of this ubiquitous environmental influence on hypertension, associated organ damage and the microbiome.
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