ArticleInnate immunity2019
Organic dust inhibits surfactant protein expression by reducing thyroid transcription factor-1 levels in human lung epithelial cells.
Article in Innate immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Redox-sensitive GPCR signaling drives Gq-dependent CaAmerican journal of physiology. Cell physiology · 2026Article
- The Na/K-ATPase role as a signal transducer in lung inflammation.Frontiers in immunology · 2023Review
- Bacterial extracellular vesicles isolated from organic dust induce neutrophilic inflammation in the lung.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Is Progression of Pulmonary Fibrosis due to Ventilation-induced Lung Injury?American journal of respiratory and critical care medicine · 2019Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Exposure to organic dust is a risk factor for the development of respiratory diseases. Surfactant proteins (SP) reduce alveolar surface tension and modulate innate immune responses to control lung inflammation. Therefore, changes in SP levels could contribute to the development of organic-dust-induced respiratory diseases. Because information on the effects of organic dust on SP levels is lacking, we studied the effects of dust from a poultry farm on SP expression. We found that dust extract reduced SP-A and SP-B mRNA and protein levels in H441 human lung epithelial cells by inhibiting their promoter activities, but did not have any effect on SP-D protein levels. Dust extract also reduced SP-A and SP-C levels in primary human alveolar epithelial cells. The inhibitory effects were not due to LPS or protease activities present in dust extract or mediated via oxidative stress, but were dependent on a heat-labile factor(s). Thyroid transcription factor-1, a key transcriptional activator of SP expression, was reduced in dust-extract-treated cells, indicating that its down-regulation mediates inhibition of SP levels. Our study implies that down-regulation of SP levels by organic dust could contribute to the development of lung inflammation and respiratory diseases in humans.
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Registered trials
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