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Deciphering the Links: Fragmented Polystyrene as a Driver of Skin Inflammation

ABSTRACT: Recent studies have identified the pervasive presence of nano- and microplastics (NMP) in atmospheric air, leading to inevitable human exposure. Human skin, with an extensive surface area of 1.5-2 m², is constantly exposed to airborne NMP, yet the dermal implications of such exposure remain elusive. Our investigation employed fragmented polystyrene (fPS), a plastic commonly found in the air, to evaluate dermal penetration using various skin models. We utilized pyrolysis-gas chromatography/mass spectrometry (py-GC/MS) to quantify fPS that had penetrated the skin model. Furthermore, we examined the biological alterations in skin keratinocytes consequent to fPS exposure and analyzed the regulation of inflammatory response markers. Our findings reveal deleterious effects on skin keratinocytes, underlining the potential risks posed by short-term fPS exposure. This multifaceted skin model study offers new perspectives on the toxicological impacts of NMP.

ORGANISM(S): Homo sapiens

PROVIDER: GSE255709 | GEO | 2024/02/19

REPOSITORIES: GEO

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Project description:Hair follicle formation depends on reciprocal epidermal-dermal interactions and occurs during skin development, but not in adult life. This suggests that the properties of dermal fibroblasts change during postnatal development. To examine this, we used a PdgfraEGFP mouse line to isolate GFP-positive fibroblasts from neonatal skin, adult telogen and anagen skin and adult skin in which ectopic hair follicles had been induced (EF skin) by transgenic epidermal activation of beta-catenin. We also isolated epidermal cells from each mouse. The gene expression profile of EF epidermis was most similar to that of anagen epidermis, consistent with activation of beta-catenin signalling. In contrast, adult dermis with ectopic hair follicles more closely resembled neonatal dermis than adult telogen or anagen dermis. In particular, genes associated with mitosis were upregulated and extracellular matrix-associated genes were downregulated in neonatal and EF fibroblasts. We confirmed that sustained epidermal beta-catenin activation stimulated fibroblasts to proliferate to reach the high cell density of neonatal skin. In addition, the extracellular matrix was comprehensively remodelled, with mature collagen being replaced by collagen subtypes normally present only in developing skin. The changes in proliferation and extracellular matrix composition originated from a specific subpopulation of fibroblasts located beneath the sebaceous gland. Our results show that adult dermis is an unexpectedly plastic tissue that can be reprogrammed to acquire the molecular, cellular and structural characteristics of neonatal dermis in response to cues from the overlying epidermis. We have isolated the following populations of cells from mouse back skin by flow cytometry: 1A) GFP+ WT neonatal dermal fibroblasts, 1B) ItgA6+ WT neonatal epidermal keratinocytes, 2A) GFP+ WT telogen dermal fibroblasts, 2B) ItgA6+ WT telogen epidermal keratinocytes, 3A) GFP+ D2 transient activation (anagen) dermal fibroblasts, 3B) ItgA6+ D2 transient activation (anagen) epidermal keratinocytes, 4A) GFP+ D2 sustained activation (ectopic follicles) dermal fibroblasts, 4B) ItgA6+ D2 sustained activation (ectopic follicles) epidermal keratinocytes

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Deciphering the Links: Fragmented Polystyrene as a Driver of Skin Inflammation

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