Dataset Information

The effect of microplastics on the nasal epithelial cells in obstructive lung diseases

ABSTRACT: The goal of this study was to evaluate the biological effect of microplastic fibres on nasal epithelium from healthy subjects, as well as asthma and COPD pateients. We demonstrated the distinct biological response of asthmatic and COPD epithelial cells to microplastic fibers stimulation compared to healthy epithelial cells. ANKRD36, BCL2L15, C15orf48, CAPN14, FCGBP, FST, IL-19, MAFF, PGBD5, PKP1 and PTPRH are important markers of epithelial response after microplastic stimulation in obstructive lung disaeses. These mediators are linked to Th2 inflammation, alleviation of stress response, and, most notably, carcinogenesis. We demonstrated the distinct biological response of asthmatic and COPD epithelial cells to microplastic fibers stimulation compared to healthy epithelial cells. ANKRD36, BCL2L15, C15orf48, CAPN14, FCGBP, FST, IL-19, MAFF, PGBD5, PKP1 and PTPRH are important markers of epithelial response after microplastic stimulation in obstructive lung disaeses. These mediators are linked to Th2 inflammation, alleviation of stress response, and, most notably, carcinogenesis. Microplastic stimulation differently modified the response of airway epithelial cells in obstructive lung diseases than in controls. Asthmatic and COPD epithelial cells are more prone to damage after microplastic fibre exposure.

ORGANISM(S): Homo sapiens

PROVIDER: GSE273262 | GEO | 2025/02/12

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:The apical junctional complex (AJC), composed of tight junctions and adherens junctions, is essential for maintaining epithelial barrier function. Since cigarette smoking and chronic obstructive pulmonary disease (COPD), the major smoking-induced disease, are both associated with increased lung epithelial permeability, we hypothesized that smoking alters the transcriptional program regulating AJC integrity in the small airway epithelium (SAE), the primary site of pathological changes in COPD. Transcriptome analysis revealed a global down-regulation of physiological AJC gene expression in the SAE of healthy smokers (n=53) compared to healthy nonsmokers (n=59), an observation associated with changes in molecular pathways regulating epithelial differentiation such as PTEN signaling and accompanied by induction of cancer-related AJC genes. Genome-wide co-expression analysis identified a smoking-sensitive AJC transcriptional network. The overall expression of AJC-associated genes was further decreased in COPD smokers (n=23). Exposure of human airway epithelial cells to cigarette smoke extract in vitro resulted in down-regulation of several AJC-related genes, accompanied by decreased transepithelial resistance. Thus, cigarette smoking alters the AJC gene expression architecture in the human airway epithelium, providing a molecular basis for the dysregulation of airway epithelial barrier function during the development of smoking-induced lung disease. The apical junctional complex (AJC), composed of tight junctions and adherens junctions, is essential for maintaining epithelial barrier function. Since cigarette smoking and chronic obstructive pulmonary disease (COPD), the major smoking-induced disease, are both associated with increased lung epithelial permeability, we hypothesized that smoking alters the transcriptional program regulating AJC integrity in the small airway epithelium (SAE), the primary site of pathological changes in COPD. In this study, microarray analysis of the SAE obtained from 53 healthy nonsmokers, 59 healthy smokers, and 23 smokers with COPD was performed to determine physiological AJC gene expression architecture in the SAE and its modification by cigarette smoking and during the development of COPD.

Dataset Information

The effect of microplastics on the nasal epithelial cells in obstructive lung diseases

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets