Effects of polystyrene microbeads on cytotoxicity and transcriptomic profiles in human Caco‐2 cells

Abstract

Microplastics (MPs) pollution is a global paradigm that raises concern in relation to environment and human health. In order to investigate the molecular toxicity mechanisms of MPs, transcriptomic analyses were performed on in vitro Caco‐2 cell model. After observing that polystyrene microplastics (PS‐MPs) decreased cell viability in a dose‐dependent manner, the responsible genes and involved pathways that might make contribution to PS‐MBs‐induced toxicity to Caco‐2 cells were identified with Illumina RNA seq. A total of 442 genes including, 210 up‐regulated ones and 232 down‐regulated ones, showed differential expression after treatment by PS‐MPs with a concentration of 12.5 mg L−1 or 50.0 mg L−1 for 24 hours. Gene Ontology (GO) annotation enriched unigenes can be grouped into three separated clusters: cellular component (CC), biological process (BP), and molecular function (MF). The dominate pathways related to NF‐κB, MAPK signaling, cytokine‐cytokine receptor interaction, and toll‐like receptor were strongly influenced by PS‐MBs. These pathways are involved in modulating cell inflammatory and proliferation. The qPCR were applied to investigate the transcriptional level of five proliferation related genes (Ras, ERK, MER, CDK4, Cyclin D1) and four inflammation related genes (TRPV1, iNOS, IL‐1β, IL‐8), and the results were consistent with RNA‐seq data. This study has provided new insight into the understanding of the toxicity effects of PS‐MBs‐induced intestinal inflammatory diseases.

Epicutaneous sensitization in the development of food allergy: What is the evidence and how can this be prevented?

“…In an in vitro model of human epithelial colorectal cells, researchers found that exposure to microplastics upregulated transcriptional factors involved in cell inflammation and proliferation. The chronic exposure to low doses of microplastics has the potential to induce epithelial cell injury and alterations to intestinal barrier function 134 . In a study of human lung epithelial cells, researchers found that exposure to inhaled polystyrene microplastics causes inflammatory and oxidative injury along with the disruption of intercellular junction proteins in the lung, potentially leading to pulmonary barrier dysfunction 135 …”

Harnessing PET to track micro- and nanoplastics in vivo

“…(2019) and Rafiee et al (2018) in which translocation of PS particles from the gut was not observed and toxicologically relevant effects related to PS exposure were not found in vivo in rodents or in vitro in human intestinal epithelium 32 , 33 . Even more recently, however, several studies have suggested that microplastics can induce gut microbiota dysbiosis, intestinal barrier dysfunction, inflammation, and metabolic disorders in both mice and their offspring 34 – 46 .…”

Bibliometric Profile of Global Microplastics Research from 2004 to 2019

“…Other sources of human exposure to MPs include commercial salt and bottled drinks, as well as airborne MPs that can be inhaled [ 77 ]. Although MPs have been detected in human stool samples [ 78 ], nanoplastics reportedly might decrease the viability of human Caco-2 cells [ 79 ], and they can induce pro-inflammatory responses [ 80 ]—adverse effects of MPs on human health have not been reported to date. Thus, studies of the effects of MPs on human health are still urgently needed.…”