ArticleThorax2004
Protective role of metallothionein in acute lung injury induced by bacterial endotoxin.
Article in Thorax, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 71 citations in OpenAlex.
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- Metallothioneins in Inflammatory Bowel Diseases: Importance in Pathogenesis and Potential Therapy Target.Canadian journal of gastroenterology & hepatology · 2021Review
- Evaluation of metallothionein and Ki-67 expression in chronic cholangiohepatitis in cats.Canadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2021Article
- Food-Origin Mycotoxin-Induced Neurotoxicity: Intend to Break the Rules of Neuroglia Cells.Oxidative medicine and cellular longevity · 2021Review
- Bioinformatics Analysis Identifies Hub Genes and Molecular Pathways Involved in Sepsis-Induced Myopathy.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Exosomes from mesenchymal stromal cells reduce murine colonic inflammation via a macrophage-dependent mechanism.JCI insight · 2019Article
- Developmental Exposure of Mice to T-2 Toxin Increases Astrocytes and Hippocampal Neural Stem Cells Expressing Metallothionein.Neurotoxicity research · 2019Article
- Insights into the Signal Transduction Pathways of Mouse Lung Type II Cells Revealed by Transcription Factor Profiling in the Transcriptome.Genomics & informatics · 2019Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMetallothionein (MT) is a protein that can be induced by inflammatory mediators and participate in cytoprotection. However, its role in inflammation remains to be established. A study was undertaken to determine whether intrinsic MT protects against acute inflammatory lung injury induced by bacterial endotoxin in MT-I/II knock out (-/-) and wild type (WT) mice.
methodsMT (-/-) and WT mice were given vehicle or lipopolysaccharide (LPS, 125 microg/kg) intratracheally and the cellular profile of the bronchoalveolar lavage (BAL) fluid, pulmonary oedema, lung histology, expression of proinflammatory molecules, and nuclear localisation of nuclear factor-kappaB (NF-kappaB) in the lung were evaluated.
resultsMT (-/-) mice were more susceptible than WT mice to lung inflammation, especially to lung oedema induced by intratracheal challenge with LPS. After LPS challenge, MT deficiency enhanced vacuolar degeneration of pulmonary endothelial cells and type I alveolar epithelial cells and caused focal loss of the basement membrane. LPS treatment caused no significant differences in the enhanced expression of proinflammatory cytokines and chemokines nor in the activation of the NF-kappaB pathway in the lung between the two genotypes. Lipid peroxide levels in the lungs were significantly higher in LPS treated MT (-/-) mice than in LPS treated WT mice.
conclusionsEndogenous MT protects against acute lung injury related to LPS. The effects are possibly mediated by the enhancement of pulmonary endothelial and epithelial integrity, not by the inhibition of the NF-kappaB pathway.
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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.