ArticleToxicology and applied pharmacology2017
Arsenic alters transcriptional responses to Pseudomonas aeruginosa infection and decreases antimicrobial defense of human airway epithelial cells.
Article in Toxicology and applied pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.
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Who cites it
12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 23 citations in OpenAlex.
- Toxic metal exposure as a possible risk factor for COVID-19 and other respiratory infectious diseases.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020Pooled it
- Selection of reference genes for quantitative PCR: identifying reference genes for airway epithelial cells exposed toAmerican journal of physiology. Lung cellular and molecular physiology · 2020Pooled it
- Polymicrobial Extracellular Vesicles Reduce the Innate Immune Response of Human Cystic Fibrosis Bronchial Epithelial Cells.Journal of extracellular biology · 2026Article
- Exploring the Role ofACS infectious diseases · 2026Article
- Polymicrobial extracellular vesicles reduce the innate immune response of human cystic fibrosis bronchial epithelial cells.bioRxiv : the preprint server for biology · 2026Article
- Article
- Genome-wide mapping of gene-microbe interactions in the murine lung microbiota based on quantitative microbial profiling.Animal microbiome · 2023Article
- Somatic cell hemoglobin modulates nitrogen oxide metabolism in the human airway epithelium.Scientific reports · 2021Article
- A functional genomics approach to investigate the differentiation of iPSCs into lung epithelium at air-liquid interface.Journal of cellular and molecular medicine · 2020Article
- Single-cell RNA-seq Analysis Reveals That Prenatal Arsenic Exposure Results in Long-term, Adverse Effects on Immune Gene Expression in Response to Influenza A Infection.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- High-throughput sequencing reveals the gut and lung prokaryotic community profiles of the Chinese giant salamander (Andrias davidianus).Molecular biology reports · 2019Article
- Cell function and identity revealed by comparative scRNA-seq analysis in human nasal, bronchial and epididymis epithelia.European journal of cell biologyArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Arsenic contamination of drinking water and food threatens the health of hundreds of millions of people worldwide by increasing the risk of numerous diseases. Arsenic exposure has been associated with infectious lung disease in epidemiological studies, but it is not yet understood how ingestion of low levels of arsenic increases susceptibility to bacterial infection. Accordingly, the goal of this study was to examine the effect of arsenic on gene expression in primary human bronchial epithelial (HBE) cells and to determine if arsenic altered epithelial cell responses to Pseudomonas aeruginosa, an opportunistic pathogen. Bronchial epithelial cells line the airway surface, providing a physical barrier and serving critical roles in antimicrobial defense and signaling to professional immune cells. We used RNA-seq to define the transcriptional response of HBE cells to Pseudomonas aeruginosa, and investigated how arsenic affected HBE gene networks in the presence and absence of the bacterial challenge. Environmentally relevant levels of arsenic significantly changed the expression of genes involved in cellular redox homeostasis and host defense to bacterial infection, and decreased genes that code for secreted antimicrobial factors such as lysozyme. Using pathway analysis, we identified Sox4 and Nrf2-regulated gene networks that are predicted to mediate the arsenic-induced decrease in lysozyme secretion. In addition, we demonstrated that arsenic decreased lysozyme in the airway surface liquid, resulting in reduced lysis of Microccocus luteus. Thus, arsenic alters the expression of genes and proteins in innate host defense pathways, thereby decreasing the ability of the lung epithelium to fight bacterial infection.
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