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#5502 Pro-inflammatory Effects of Bisphenol a and Polyethylene Microplastics on Human Renal Tubular Cells
Summary
Laboratory experiments showed that both bisphenol A (BPA) and polyethylene microplastics activate inflammatory pathways in human kidney tubular cells, and their combination amplifies this effect through the so-called "Trojan Horse" mechanism. Exposure triggered the aryl hydrocarbon receptor and elevated pro-inflammatory cytokines linked to kidney fibrosis. These findings suggest that combined exposure to microplastics and chemical additives may contribute to the rising global burden of chronic kidney disease.
Abstract Background Growing evidence shows that microplastics (MP) and their chemical derivates contaminate the environment and accumulate in the gut, liver, lungs, and kidneys. Furthermore, MP can adsorb a wide range of toxic substances (heavy metals, polycyclic aromatic hydrocarbons, Bisphenol A [B]), causing the accumulation of multiple pollutants and so, enhancing their toxicity (the so-called “Trojan Horse” effect). An epidemic of chronic kidney disease (CKD) of uncertain etiology is emerging worldwide and understanding the involvement of environmental pollution may be critical for health policies and public health responses. Inflammation is intimately linked to renal disease, and proinflammatory cytokines and chemokines are important mediators of fibrosis in the tubulointerstitial compartments. Aims To evaluate the effects of B and Polyethylene (Pe)-MPs and their combination B+Pe-MP on human renal tubular cells (HK-2). To this end, the activation of the Aryl hydrocarbon Receptor (AHR), a transcription factor binding xenobiotics, and the expression of inflammatory molecules were explored. Method HK-2 were exposed to 0 (No Treated cells: NT), 100 nM B, 0.2 mg/ml Pe-MP (diameter 1-4 µm), and B+Pe-MP for 5-24 hrs. Cell uptake of (FL)uorescent Pe-MP was visualized by microscope; viability was assessed by MTT; AHR, HSP90, CCL2, CCR2, CCL5, and CCR5 expression was studied by rt-PCR, Western blot, and immunofluorescence Results After 5 hrs exposure, a FLPe-MP cytoplasmatic and perinuclear deposition was observed (Figure 1). After 24 hrs, Pe-MP and B+Pe-MP exposition reduced cell viability (−20% vs NT p < 0.001). The treatments increased AHR expression (1.5-3-fold vs NT, p < 0.05-0.001), which had a nuclear localization both at 5 and 24 hrs. Conversely, HSP90 expression, a chaperone that keeps AHR inactive, decreased (−20-40% vs NT, p < 0.05) (Figure 2). After 5 hrs, CCL2 levels rose (1.8-3.5 fold, p<0.05-0.0001 vs NT) as well as its receptor CCR2 (2.3-6.7 fold, p<0.05-0.01). Similarly, CCL5 and CCR5 were, respectively, 1.6-2.7 and 3.8-8.4 fold overexpressed with respect to NT (p < 0.05-0.01). Interestingly, the co-exposure significantly enhanced the expression of these inflammatory molecules Conclusion Our data suggest that B and Pe-MPs induce a pro-inflammatory response in renal tubular cells and that the combined effect of B and Pe-MPs induces a worse effect on HK2 than B or MPs alone, supporting the theory of the “trojan horse” effect mediated by MPs. Therefore, MPs could be a trigger of kidney damage, thus confirming the potential impact of the environment on the pathogenesis of the renal disease. Moreover, these data could address the importance of investigating any health implications associated with MPs.
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