ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2012
Lipopolysaccharide-induced cyclooxygenase-2 expression in mouse transformed Clara cells.
Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
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- Cyclooxygenase-2 deficiency attenuates lipopolysaccharide-induced inflammation, apoptosis, and acute lung injury in adult mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
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- Article
- Macrophage inflammatory protein-2 as mediator of inflammation in acute liver injury.World journal of gastroenterology · 2017Review
- Post-Intake of S-Ethyl Cysteine and S-Methyl Cysteine Improved LPS-Induced Acute Lung Injury in Mice.Nutrients · 2016Article
- The thioredoxin reductase-1 inhibitor aurothioglucose attenuates lung injury and improves survival in a murine model of acute respiratory distress syndrome.Antioxidants & redox signaling · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND/
aimsExacerbation of innate immune responses can contribute to development of acute lung injury. Multiple cell populations, including the bronchiolar epithelium, coordinate these inflammatory responses. Clara cells, non-ciliated epithelial cells, are located in the distal airways in humans and conducting airways in mice. These cells actively participate in innate immune responses but their precise contributions remain poorly defined.
methodsTo test the hypothesis that E. coli lipopolysaccaride (LPS) treatment stimulates production of pro-inflammatory mediators in mouse transformed Clara cells (MTCC), MTCC were treated with E. coli lipopolysaccaride (LPS).
resultsLPS increased COX-2 expression and stimulated production of prostaglandins, including prostaglandin E(2) (PGE(2)). Enhanced mitogen activated protein kinase (MAPK) activation, nuclear factor-κB (NFκB) activation, and chemokine production were observed in MTCC in response to LPS treatment.
conclusionsWhile the role for Clara cells in the regulation of host defense and the progression of acute lung injury needs further characterization, our data suggests the importance of this unique cell population in the pathogenesis of LPS-induced acute lung injury.
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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.