ArticleAmerican journal of respiratory cell and molecular biology2012
Chronic endotoxin exposure produces airflow obstruction and lung dendritic cell expansion.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- TLR/NF-κB activation in vitro as a tool in the assessment of occupational bioaerosol exposure and health risks in wastewater treatment plants.Journal of exposure science & environmental epidemiology · 2026Article
- Proteomic profiling reveals immunologic mediators of endotoxin-related lung function decline: a longitudinal prospective study in textile workers.Respiratory research · 2026Article
- A cross-sectional study on occupational exposure to microorganisms, endotoxin, hydrogen sulfide, and dust during work at drilling waste treatment plants.Annals of work exposures and health · 2024Article
- Animal models: An essential tool to dissect the heterogeneity of chronic obstructive pulmonary disease.Journal of translational internal medicine · 2023Article
- Assessment of airborne endotoxin in sandstorm dust and indoor environments using a novel passive sampling device in Al Zulfi city, Saudi Arabia - Establishing threshold exposure levels.Saudi journal of biological sciences · 2021Article
- Associations Between Bioaerosol Exposures and Lung Function Changes Among Dairy Workers in Colorado.Journal of occupational and environmental medicine · 2020Article
- Microbial Toxins in E-Liquid: A Potential New Vaping-Related Exposure to Explore.Environmental health perspectives · 2019Article
- CFTR regulates B cell activation and lymphoid follicle development.Respiratory research · 2019Article
- Endotoxin andEnvironmental health perspectives · 2019Article
- Sirtuin 2 enhances allergic asthmatic inflammation.JCI insight · 2019Article
- Imaging Phenotype of Occupational Endotoxin-Related Lung Function Decline.Environmental health perspectives · 2016Article
- Risks associated with endotoxins in feed additives produced by fermentation.Environmental health : a global access science source · 2016Review
- Endotoxin and gender modify lung function recovery after occupational organic dust exposure: a 30-year study.Occupational and environmental medicine · 2015Article
- Isoflurane Ameliorates Acute Lung Injury by Preserving Epithelial Tight Junction Integrity.Anesthesiology · 2015Article
- Dendritic cell-bound IgE functions to restrain allergic inflammation at mucosal sites.Mucosal immunology · 2015Article
- Long-term respiratory health effects in textile workers.Current opinion in pulmonary medicine · 2013Review
- Integrating murine gene expression studies to understand obstructive lung disease due to chronic inhaled endotoxin.PloS one · 2013Article
- Respiratory problems among cotton textile workers.Lung India : official organ of Indian Chest SocietyArticle
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Little is known about the mechanisms of persistent airflow obstruction that result from chronic occupational endotoxin exposure. We sought to analyze the inflammatory response underlying persistent airflow obstruction as a result of chronic occupational endotoxin exposure. We developed a murine model of daily inhaled endotoxin for periods of 5 days to 8 weeks. We analyzed physiologic lung dysfunction, lung histology, bronchoalveolar lavage fluid and total lung homogenate inflammatory cell and cytokine profiles, and pulmonary gene expression profiles. We observed an increase in airway hyperresponsiveness as a result of chronic endotoxin exposure. After 8 weeks, the mice exhibited an increase in bronchoalveolar lavage and lung neutrophils that correlated with an increase in proinflammatory cytokines. Detailed analyses of inflammatory cell subsets revealed an expansion of dendritic cells (DCs), and in particular, proinflammatory DCs, with a reduced percentage of macrophages. Gene expression profiling revealed the up-regulation of a panel of genes that was consistent with DC recruitment, and lung histology revealed an accumulation of DCs in inflammatory aggregates around the airways in 8-week-exposed animals. Repeated, low-dose LPS inhalation, which mirrors occupational exposure, resulted in airway hyperresponsiveness, associated with a failure to resolve the proinflammatory response, an inverted macrophage to DC ratio, and a significant rise in the inflammatory DC population. These findings point to a novel underlying mechanism of airflow obstruction as a result of occupational LPS exposure, and suggest molecular and cellular targets for therapeutic development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.