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Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis.
Environ Epigenet
January 2025
Institute of Human Genetics, School of Medicine, Pontificia Universidad Javeriana, Bogotá 110231, Colombia.
Fine particulate matter (PM), an atmospheric pollutant that settles deep in the respiratory tract, is highly harmful to human health. Despite its well-known impact on lung function and its ability to exacerbate asthma, the molecular basis of this effect is not fully understood. This integrated transcriptomic and epigenomic data analysis from publicly available datasets aimed to determine the impact of PM exposure and its association with asthma in human airway epithelial cells.
View Article and Find Full Text PDF17q21 Variants Disturb Mucosal Host Defense in Childhood Asthma.
Am J Respir Crit Care Med
April 2024
Center of Allergy and Environment (ZAUM), Technical University and Helmholtz Center Munich, Munich, Germany.
The strongest genetic risk factor for childhood-onset asthma, the 17q21 locus, is associated with increased viral susceptibility and disease-promoting processes. To identify biological targets underlying the escalated viral susceptibility associated with the clinical phenotype mediated by the 17q21 locus. Genome-wide transcriptome analysis of nasal brush samples from 261 children (78 healthy, 79 with wheezing at preschool age, 104 asthmatic) within the ALLIANCE (All-Age-Asthma) cohort, with a median age of 10.
View Article and Find Full Text PDFMechanisms of airway epithelial injury and abnormal repair in asthma and COPD.
Front Immunol
August 2023
National Heart and Lung Institute, Imperial College London, London, United Kingdom.
The airway epithelium comprises of different cell types and acts as a physical barrier preventing pathogens, including inhaled particles and microbes, from entering the lungs. Goblet cells and submucosal glands produce mucus that traps pathogens, which are expelled from the respiratory tract by ciliated cells. Basal cells act as progenitor cells, differentiating into different epithelial cell types, to maintain homeostasis following injury.
View Article and Find Full Text PDFEpigenetics of asthma-the field continues to evolve.
Ann Transl Med
November 2022
Children's National Hospital, George Washington University School of Medicine and Health Sciences, Washington, DC, USA.
MBD2 mediates Th17 cell differentiation by regulating MINK1 in Th17-dominant asthma.
Front Genet
October 2022
Department of Emergency, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
.Asthma is a highly heterogeneous disease, and T-helper cell type 17 (Th17) cells play a pathogenic role in the development of non-T2 severe asthma. Misshapen like kinase 1 (MINK1) is involved in the regulation of Th17 cell differentiation, but its effect on severe asthma remains unclear.
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