ArticleAmerican journal of respiratory cell and molecular biology2009
The systemic inflammation of alveolar hypoxia is initiated by alveolar macrophage-borne mediator(s).
Article in American journal of respiratory cell and molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 56 citations in OpenAlex.
- A high fraction of inspired oxygen does not mitigate atelectasis-induced lung tissue hypoxia or injury in experimental acute respiratory distress syndrome.Scientific reports · 2025Article
- Analysis of hub genes temporal dynamics in cardiac ischemia/reperfusion injury: a bioinformatics and experimental study.Frontiers in physiology · 2025Article
- Acute or chronic pulmonary emphysema? Or both?-A contribution to the diagnosis of death due to violent asphyxiation in cases with pre-existing chronic emphysema.International journal of legal medicine · 2022Article
- Review
- Chronic Obstructive Pulmonary Disease and the Cardiovascular System: Vascular Repair and Regeneration as a Therapeutic Target.Frontiers in cardiovascular medicine · 2021Review
- Cellular and Molecular Effects of SARS-CoV-2 Linking Lung Infection to the Brain.Frontiers in immunology · 2021Review
- The Impact of Hypoxia on Neutrophil Degranulation and Consequences for the Host.International journal of molecular sciences · 2020Review
- Decreased Ambient Oxygen Tension Alters the Expression of Endothelin-1, iNOS and cGMP in Rat Alveolar Macrophages.International journal of medical sciences · 2019Article
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- MCPIP1-induced autophagy mediates ischemia/reperfusion injury in endothelial cells via HMGB1 and CaSR.Scientific reports · 2018Article
- Acclimatization of the systemic microcirculation to alveolar hypoxia is mediated by an iNOS-dependent increase in nitric oxide availability.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Article
- MCPIP1 Regulates Alveolar Macrophage Apoptosis and Pulmonary Fibroblast Activation After in vitro Exposure to Silica.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Atelectasis causes alveolar hypoxia-induced inflammation during uneven mechanical ventilation in rats.Intensive care medicine experimental · 2015Article
- p53/PUMA expression in human pulmonary fibroblasts mediates cell activation and migration in silicosis.Scientific reports · 2015Article
- Nitric oxide and superoxide anion balance in rats exposed to chronic and long term intermittent hypoxia.BioMed research international · 2014Article
- Dexamethasone blocks the systemic inflammation of alveolar hypoxia at several sites in the inflammatory cascade.American journal of physiology. Heart and circulatory physiology · 2012Article
- Chronic hypoxia-induced acid-sensitive ion channel expression in chemoafferent neurons contributes to chemoreceptor hypersensitivity.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Renin released from mast cells activated by circulating MCP-1 initiates the microvascular phase of the systemic inflammation of alveolar hypoxia.American journal of physiology. Heart and circulatory physiology · 2011Article
- Alveolar macrophages initiate the systemic microvascular inflammatory response to alveolar hypoxia.Respiratory physiology & neurobiology · 2011Review
- Monocyte chemoattractant protein-1 released from alveolar macrophages mediates the systemic inflammation of acute alveolar hypoxia.American journal of respiratory cell and molecular biology · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alveolar hypoxia produces widespread systemic inflammation in rats. The inflammation appears to be triggered by activation of mast cells by a mediator released from alveolar macrophages, not by the reduced systemic partial pressure of oxygen (PO2). If this is correct, the following should apply: (1) neither mast cells nor tissue macrophages should be directly activated by hypoxia; and (2) mast cells should be activated when in contact with hypoxic alveolar macrophages, but not with hypoxic tissue macrophages. We sought here to determine whether hypoxia activates isolated alveolar macrophages, peritoneal macrophages, and peritoneal mast cells, and to study the response of the microcirculation to supernatants of these cultures. Rat mesenteric microcirculation intravital microscopy was combined with primary cultures of alveolar macrophages, peritoneal macrophages, and peritoneal mast cells. Supernatant of hypoxic alveolar macrophages, but not of hypoxic peritoneal macrophages, produced inflammation in mesentery. Hypoxia induced a respiratory burst in alveolar, but not peritoneal macrophages. Cultured peritoneal mast cells did not degranulate with hypoxia. Immersion of mast cells in supernatant of hypoxic alveolar macrophages, but not in supernatant of hypoxic peritoneal macrophages, induced mast cell degranulation. Hypoxia induced release of monocyte chemoattractant protein-1, a mast cell secretagogue, from alveolar, but not peritoneal macrophages or mast cells. We conclude that a mediator released by hypoxic alveolar macrophages activates mast cells and triggers systemic inflammation. Reduced systemic PO2 and activation of tissue macrophages do not play a role in this phenomenon. The inflammation could contribute to systemic effects of diseases featuring alveolar hypoxia.
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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.