ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Macrophage TNF-α mediates parathion-induced airway hyperreactivity in guinea pigs.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Exploration of the mechanism of Qi-Xian decoction in asthmatic mice using metabolomics combined with network pharmacology.Frontiers in molecular biosciences · 2023Article
- Organophosphorus pesticides exhibit compound specific effects in rat precision-cut lung slices (PCLS): mechanisms involved in airway response, cytotoxicity, inflammatory activation and antioxidative defense.Archives of toxicology · 2022Article
- Effects of Chlorpyrifos on Serine Hydrolase Activities, Lipid Mediators, and Immune Responses in Lungs of Neonatal and Adult Mice.Chemical research in toxicology · 2021Article
- Mini review: Neural mechanisms underlying airway hyperresponsiveness.Neuroscience letters · 2021Review
- Study of ethion and lipopolysaccharide interaction on lung in a mouse model.Laboratory animal research · 2020Article
- Organophosphorus Pesticides Induce Cytokine Release from Differentiated Human THP1 Cells.American journal of respiratory cell and molecular biology · 2019Article
- Mechanisms of organophosphorus pesticide toxicity in the context of airway hyperreactivity and asthma.American journal of physiology. Lung cellular and molecular physiology · 2018Review
- The Organophosphorus Pesticide Chlorpyrifos Induces Sex-Specific Airway Hyperreactivity in Adult Rats.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Oral exposure of deltamethrin and/or lipopolysaccharide (LPS) induced activation of the pulmonary immune system in Swiss albino mice.Environmental science and pollution research international · 2018Article
- Pesticide dichorvos induces early solid Ehrlich tumoral development associated with a non-protective pro-inflammatory response.Environmental science and pollution research international · 2018Article
- Ozone-induced eosinophil recruitment to airways is altered by antigen sensitization and tumor necrosis factor-Physiological reports · 2017Article
- Newly divided eosinophils limit ozone-induced airway hyperreactivity in nonsensitized guinea pigs.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Protective Role of Eosinophils and TNFa after Ozone Inhalation.Research report (Health Effects Institute) · 2017Article
- The influence of sensitization on mechanisms of organophosphorus pesticide-induced airway hyperreactivity.American journal of respiratory cell and molecular biology · 2015Article
- Early-life exposure to organophosphate pesticides and pediatric respiratory symptoms in the CHAMACOS cohort.Environmental health perspectives · 2015Article
- Respiratory disease in United States farmers.Occupational and environmental medicine · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Organophosphorus pesticides (OPs) are implicated in human asthma. We previously demonstrated that, at concentrations that do not inhibit acetylcholinesterase activity, the OP parathion causes airway hyperreactivity in guinea pigs as a result of functional loss of inhibitory M2 muscarinic receptors on parasympathetic nerves. Because macrophages are associated with asthma, we investigated whether macrophages mediate parathion-induced M2 receptor dysfunction and airway hyperreactivity. Airway physiology was measured in guinea pigs 24 h after a subcutaneous injection of parathion. Pretreatment with liposome-encapsulated clodronate induced alveolar macrophage apoptosis and prevented parathion-induced airway hyperreactivity in response to electrical stimulation of the vagus nerves. As determined by qPCR, TNF-α and IL-1β mRNA levels were increased in alveolar macrophages isolated from parathion-treated guinea pigs. Parathion treatment of alveolar macrophages ex vivo did not significantly increase IL-1β and TNF-α mRNA but did significantly increase TNF-α protein release. Consistent with these data, pretreatment with the TNF-α inhibitor etanercept but not the IL-1β receptor inhibitor anakinra prevented parathion-induced airway hyperreactivity and protected M2 receptor function. These data suggest a novel mechanism of OP-induced airway hyperreactivity in which low-level parathion activates macrophages to release TNF-α-causing M2 receptor dysfunction and airway hyperreactivity. These observations have important implications regarding therapeutic approaches for treating respiratory disease associated with OP exposures.
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