ArticleAmerican journal of respiratory cell and molecular biology2011
Monocyte chemoattractant protein-1 released from alveolar macrophages mediates the systemic inflammation of acute alveolar hypoxia.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Pooled it
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- Major pathophysiological changes in pulmonary disease provided a molecular insight based on deep learning approach.Scientific reports · 2025Article
- 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
- Immunoregulatory Macrophages Modify Local Pulmonary Immunity and Ameliorate Hypoxic Pulmonary Hypertension.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Valproate-Induced Metabolic Syndrome.Biomedicines · 2023Review
- Renin-angiotensin-system inhibitors and the risk of exacerbations in chronic obstructive pulmonary disease: a nationwide registry study.BMJ open respiratory research · 2023Article
- Article
- Assessing the impact of gestational age of donors on the efficacy of amniotic epithelial cell-derived extracellular vesicles in experimental bronchopulmonary dysplasia.Stem cell research & therapy · 2022Article
- Optimal Management of Heart Failure and Chronic Obstructive Pulmonary Disease: Clinical Challenges.International journal of general medicine · 2022Review
- The Association of Renin-Angiotensin System Blockades and Mortality in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease and Acute Respiratory Failure: A Retrospective Cohort Study.International journal of chronic obstructive pulmonary disease · 2022Article
- 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
- Genetic Variants, Circulating Level of MCP1 with Risk of Chronic Obstructive Pulmonary Disease: A Case-Control Study.Pharmacogenomics and personalized medicine · 2021Article
- The chemokine receptor antagonist cenicriviroc inhibits the replication of SARS-CoV-2 in vitro.Antiviral research · 2020Article
- 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
- A Time- and Compartment-Specific Activation of Lung Macrophages in Hypoxic Pulmonary Hypertension.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- The impact of inflammation on respiratory plasticity.Experimental neurology · 2017Review
- 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
- Are mast cells implicated in asphyxia?International journal of legal medicine · 2016Article
- Atelectasis causes alveolar hypoxia-induced inflammation during uneven mechanical ventilation in rats.Intensive care medicine experimental · 2015Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alveolar hypoxia produces rapid systemic inflammation in rats. Several lines of evidence suggest that the inflammation is not initiated by low systemic tissue partial pressure of oxygen (Po(2)) but by a mediator released into the circulation by hypoxic alveolar macrophages. The mediator activates tissue mast cells to initiate inflammation. Monocyte chemoattractant protein-1/Chemokine (C-C motif) ligand 2 (MCP-1/CCL2) is rapidly released by hypoxic alveolar macrophages. This study investigated whether MCP-1 is the mediator of the systemic inflammation of alveolar hypoxia. Experiments in rats and in alveolar macrophages and peritoneal mast cells led to several results. (1) Alveolar hypoxia (10% O(2) breathing, 60 minutes) produced a rapid (5-minute) increase in plasma MCP-1 concentrations in conscious intact rats but not in alveolar macrophage-depleted rats. (2) Degranulation occurred when mast cells were immersed in the plasma of hypoxic intact rats but not in the plasma of alveolar macrophage-depleted rats. (3) MCP-1 added to normoxic rat plasma and the supernatant of normoxic alveolar macrophages produced a concentration-dependent degranulation of immersed mast cells. (4) MCP-1 applied to the mesentery of normoxic intact rats replicated the inflammation of alveolar hypoxia. (5) The CCR2b receptor antagonist RS-102895 prevented the mesenteric inflammation of alveolar hypoxia in intact rats. Additional data suggest that a cofactor constitutively generated in alveolar macrophages and present in normoxic body fluids is necessary for MCP-1 to activate mast cells at biologically relevant concentrations. We conclude that alveolar macrophage-borne MCP-1 is a key agent in the initiation of the systemic inflammation of alveolar hypoxia.
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