ArticleAmerican journal of physiology. Lung cellular and molecular physiology2002
Activation of type II alveolar epithelial cells during acute endotoxemia.
Article in American journal of physiology. Lung cellular and molecular physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Neutrophils, not macrophages, aid phage-mediated control of pulmonaryFrontiers in immunology · 2025Article
- Exosomes Derived From Alveolar Epithelial Cells Promote Alveolar Macrophage Activation Mediated by miR-92a-3p in Sepsis-Induced Acute Lung Injury.Frontiers in cellular and infection microbiology · 2021Article
- Protective Role of Surfactant Protein-D Against Lung Injury and Oxidative Stress Induced by Nitrogen Mustard.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Alveolar Epithelial Cell-Derived Mediators: Potential Direct Regulators of Large Airway and Vascular Responses.American journal of respiratory cell and molecular biology · 2017Review
- Pneumonia-induced sepsis in mice: temporal study of inflammatory and cardiovascular parameters.International journal of experimental pathology · 2013Article
- Distinct responses of lung and liver macrophages to acute endotoxemia: role of toll-like receptor 4.Experimental and molecular pathology · 2013Article
- Acute endotoxemia is associated with upregulation of lipocalin 24p3/Lcn2 in lung and liver.Experimental and molecular pathology · 2007Article
- Pulmonary effects of inhaled limonene ozone reaction products in elderly rats.Toxicology and applied pharmacology · 2007Article
- Science review: redox and oxygen-sensitive transcription factors in the regulation of oxidant-mediated lung injury: role for hypoxia-inducible factor-1alpha.Critical care (London, England) · 2003Review
- Toll-like receptor 2 is expressed by alveolar epithelial cells type II and macrophages in the human lung.Histochemistry and cell biology · 2003Article
- Science review: Redox and oxygen-sensitive transcription factors in the regulation of oxidant-mediated lung injury: role for nuclear factor-kappaB.Critical care (London, England) · 2002Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Lung injury induced by acute endotoxemia is associated with increased generation of inflammatory mediators such as nitric oxide and eicosanoids, which have been implicated in the pathophysiological process. Although production of these mediators by alveolar macrophages (AM) has been characterized, the response of type II cells is unknown and was assessed in the present studies. Acute endotoxemia caused a rapid (within 1 h) and prolonged (up to 48 h) induction of nitric oxide synthase-2 (NOS-2) in type II cells but a delayed response in AM (12-24 h). In both cell types, this was associated with increased nitric oxide production. Although type II cells, and to a lesser extent AM, constitutively expressed cyclooxygenase-2, acute endotoxemia did not alter this activity. Endotoxin administration had no effect on mitogen-activated protein kinase or protein kinase B-alpha (PKB-alpha) expression. However, increases in phosphoinositide 3-kinase and phospho-PKB-alpha were observed in type II cells. The finding that this was delayed for 12-24 h suggests that these proteins do not play a significant role in the regulation of NOS-2 in this model. After endotoxin administration to rats, a rapid (within 1-2 h) activation of nuclear factor-kappaB was observed. This response was transient in type II cells but was sustained in AM. Interferon regulatory factor-1 (IRF-1) was also activated rapidly in type II cells. In contrast, IRF-1 activation was delayed in AM. These data demonstrate that type II cells, like AM, are highly responsive during acute endotoxemia and may contribute to pulmonary inflammation.
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