ArticleRespiratory research2008
Role of pulmonary intravascular macrophages in endotoxin-induced lung inflammation and mortality in a rat model.
Article in Respiratory research, 2008. 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, 45 citations in OpenAlex.
- Recruitment of pulmonary intravascular macrophages in SARS-CoV-2 infected hamsters.Cell and tissue research · 2025Article
- Exercise preconditioning and resveratrol reduce the susceptibility of rats with obstructive jaundice to endotoxin and alleviate lung injury.Frontiers in immunology · 2024Article
- Pulmonary inflammation, oxidative stress, and fibrosis in a mouse model of cholestasis: the potential protective properties of the dipeptide carnosine.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- The role of lung macrophages in acute respiratory distress syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Combating Complement's Deleterious Effects on Nanomedicine by Conjugating Complement Regulatory Proteins to Nanoparticles.Advanced materials (Deerfield Beach, Fla.) · 2022Article
- Lysophosphatidylcholine Alleviates Acute Lung Injury by Regulating Neutrophil Motility and Neutrophil Extracellular Trap Formation.Frontiers in cell and developmental biology · 2022Article
- Integrin alpha-v/beta3 expression in equine lungs and jejunum.Canadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2020Article
- Porcine Alveolar Macrophage-like cells are pro-inflammatory Pulmonary Intravascular Macrophages that produce large titers of Porcine Reproductive and Respiratory Syndrome Virus.Scientific reports · 2018Article
- Unintended effects of drug carriers: Big issues of small particles.Advanced drug delivery reviews · 2018Review
- Cholic Acid Enhances Visceral Adiposity, Atherosclerosis and Nonalcoholic Fatty Liver Disease in Microminipigs.Journal of atherosclerosis and thrombosis · 2017Article
- Expression of von Willebrand factor, pulmonary intravascular macrophages, and Toll-like receptors in lungs of septic foals.Journal of veterinary science · 2017Article
- Gadolinium chloride improves the course of TNBS and DSS-induced colitis through protecting against colonic mucosal inflammation.Scientific reports · 2014Article
- The lung in liver disease: old problem, new concepts.Transactions of the American Clinical and Climatological Association · 2013Article
- Hepatopulmonary syndrome: update on pathogenesis and clinical features.Nature reviews. Gastroenterology & hepatology · 2012Review
- Regulation of monocyte subset proinflammatory responses within the lung microvasculature by the p38 MAPK/MK2 pathway.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- What is the clinical relevance of different lung compartments?BMC pulmonary medicine · 2009Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBile-duct ligated (BDL) rats recruit pulmonary intravascular macrophages (PIMs) and are highly susceptible to endotoxin-induced mortality. The mechanisms of this enhanced susceptibility and mortality in BDL rats, which are used as a model of hepato-pulmonary syndrome, remain unknown. We tested a hypothesis that recruited PIMs promote endotoxin-induced mortality in a rat model.
methodsRats were subjected to BDL to induce PIM recruitment followed by treatment with gadolinium chloride (GC) to deplete PIMs. Normal and BDL rats were treated intravenously with E. coli lipopolysaccharide (LPS) with or without GC pre-treatment followed by collection and analyses of lungs for histopathology, electron microscopy and cytokine quantification.
resultsBDL rats recruited PIMs without any change in the expression of IL-1beta, TNF-alpha and IL-10. GC caused reduction in PIMs at 48 hours post-treatment (P < 0.05). BDL rats treated intravenously with E. coli LPS died within 3 hours of the challenge while the normal LPS-treated rats were euthanized at 6 hours after the LPS treatment. GC treatment of rats 6 hours or 48 hours before LPS challenge resulted in 80% (1/5) and 100% (0/5) survival, respectively, at 6 hours post-LPS treatment. Lungs from BDL+LPS rats showed large areas of perivascular hemorrhages compared to those pre-treated with GC. Concentrations of IL-1beta, TNF-alpha and IL-10 were increased in lungs of BDL+LPS rats compared to BDL rats treated with GC 48 hours but not 6 hours before LPS (P < 0.05).
conclusionWe conclude that PIMs increase susceptibility for LPS-induced lung injury and mortality in this model, which is blocked by a reduction in their numbers or their inactivation.
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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.