Rapid pulmonary fibrosis induced by acute lung injury via a lipopolysaccharide three-hit regimen.
Identifieur interne : 001F25 ( Ncbi/Curation ); précédent : 001F24; suivant : 001F26Rapid pulmonary fibrosis induced by acute lung injury via a lipopolysaccharide three-hit regimen.
Auteurs : Hui Li [République populaire de Chine] ; Shaohui Du ; Lina Yang ; Yangyan Chen ; Wei Huang ; Rong Zhang ; Yinghai Cui ; Jun Yang ; Dongfeng Chen ; Yiwei Li ; Saixia Zhang ; Jianhong Zhou ; Zhijun Wei ; Zhibin YaoSource :
- Innate immunity [ 1753-4259 ] ; 2009.
Descripteurs français
- KwdFr :
- Animaux, Anti-inflammatoires (pharmacologie), Antibiotiques antinéoplasiques (pharmacologie), Bléomycine (toxicité), Cytokines (), Cytokines (métabolisme), Cytokines (sang), Dexaméthasone (pharmacologie), Facteurs de transcription STAT (), Facteurs de transcription STAT (immunologie), Facteurs de transcription STAT (métabolisme), Fibrose pulmonaire (anatomopathologie), Fibrose pulmonaire (immunologie), Fibrose pulmonaire (étiologie), Hydroxyproline (analyse), Lipopolysaccharides (immunologie), Liquide de lavage bronchoalvéolaire (immunologie), Lymphocytes auxiliaires Th1 (), Lymphocytes auxiliaires Th1 (immunologie), Lymphocytes auxiliaires Th1 (métabolisme), Lymphocytes auxiliaires Th2 (), Lymphocytes auxiliaires Th2 (immunologie), Lymphocytes auxiliaires Th2 (métabolisme), Lésion pulmonaire aigüe (), Lésion pulmonaire aigüe (anatomopathologie), Lésion pulmonaire aigüe (immunologie), Modèles animaux de maladie humaine, Protéines Smad (), Protéines Smad (immunologie), Protéines Smad (métabolisme), Rat Wistar, Rats.
- MESH :
- analyse : Hydroxyproline.
- anatomopathologie : Fibrose pulmonaire, Lésion pulmonaire aigüe.
- immunologie : Facteurs de transcription STAT, Fibrose pulmonaire, Lipopolysaccharides, Liquide de lavage bronchoalvéolaire, Lymphocytes auxiliaires Th1, Lymphocytes auxiliaires Th2, Lésion pulmonaire aigüe, Protéines Smad.
- métabolisme : Cytokines, Facteurs de transcription STAT, Lymphocytes auxiliaires Th1, Lymphocytes auxiliaires Th2, Protéines Smad.
- pharmacologie : Anti-inflammatoires, Antibiotiques antinéoplasiques, Dexaméthasone.
- sang : Cytokines.
- toxicité : Bléomycine.
- étiologie : Fibrose pulmonaire.
- Animaux, Cytokines, Facteurs de transcription STAT, Lymphocytes auxiliaires Th1, Lymphocytes auxiliaires Th2, Lésion pulmonaire aigüe, Modèles animaux de maladie humaine, Protéines Smad, Rat Wistar, Rats.
English descriptors
- KwdEn :
- Acute Lung Injury (chemically induced), Acute Lung Injury (complications), Acute Lung Injury (immunology), Acute Lung Injury (pathology), Animals, Anti-Inflammatory Agents (pharmacology), Antibiotics, Antineoplastic (pharmacology), Bleomycin (toxicity), Bronchoalveolar Lavage Fluid (immunology), Cytokines (blood), Cytokines (drug effects), Cytokines (metabolism), Dexamethasone (pharmacology), Disease Models, Animal, Hydroxyproline (analysis), Lipopolysaccharides (immunology), Pulmonary Fibrosis (etiology), Pulmonary Fibrosis (immunology), Pulmonary Fibrosis (pathology), Rats, Rats, Wistar, STAT Transcription Factors (drug effects), STAT Transcription Factors (immunology), STAT Transcription Factors (metabolism), Smad Proteins (drug effects), Smad Proteins (immunology), Smad Proteins (metabolism), Th1 Cells (drug effects), Th1 Cells (immunology), Th1 Cells (metabolism), Th2 Cells (drug effects), Th2 Cells (immunology), Th2 Cells (metabolism).
- MESH :
- chemical , analysis : Hydroxyproline.
- chemical , blood : Cytokines.
- chemical , drug effects : Cytokines, STAT Transcription Factors, Smad Proteins.
- chemical , immunology : Lipopolysaccharides, STAT Transcription Factors, Smad Proteins.
- chemical , metabolism : Cytokines, STAT Transcription Factors, Smad Proteins.
- chemical , pharmacology : Anti-Inflammatory Agents, Antibiotics, Antineoplastic, Dexamethasone.
- chemically induced : Acute Lung Injury.
- complications : Acute Lung Injury.
- drug effects : Th1 Cells, Th2 Cells.
- etiology : Pulmonary Fibrosis.
- immunology : Acute Lung Injury, Bronchoalveolar Lavage Fluid, Pulmonary Fibrosis, Th1 Cells, Th2 Cells.
- metabolism : Th1 Cells, Th2 Cells.
- pathology : Acute Lung Injury, Pulmonary Fibrosis.
- chemical , toxicity : Bleomycin.
- Animals, Disease Models, Animal, Rats, Rats, Wistar.
Abstract
Based on the common characteristic of severe acute respiratory syndrome (SARS) and highly pathogenic avian influenza and the mechanism of inflammation and fibrosis, it is speculated that there should exist a fundamental pathological rule that severe acute lung injury (ALI)-induced rapid pulmonary fibrosis is caused by various etiological factors, such as SARS coronavirus, H5N1-virus, or other unknown factors, and also by lipopolysaccharide (LPS), the most common etiological factor. The investigation employed intratracheally, and intraperitoneally and intratracheally applied LPS three-hit regimen, compared with bleomycin-induced chronic pulmonary fibrosis. Inflammatory damage and fibrosis were evaluated, and the molecular mechanism was analyzed according to Th1/Th2 balance, Sma- and MAD-related proteins (Smads) and signal transducer and activator of transcriptions (STATs) expression. The results suggested that rapid pulmonary fibrosis could be induced by ALI via LPS three-hits. The period from 3-7 days in the LPS group was the first rapid pulmonary fibrosis stage, whereas the second fast fibrosis stage occurred on days 14-21. Th2 cell polarization, Smad4 and Smad7 should be the crucial molecular mechanism of ALI-induced rapid fibrosis. The investigation was not only performed to establish a new rapid pulmonary fibrosis model, but also to provide the elicitation for mechanism of ALI changed into the rapid pulmonary fibrosis.
DOI: 10.1177/1753425908101509
PubMed: 19474208
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pubmed:19474208Le document en format XML
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<term>Acute Lung Injury (immunology)</term>
<term>Acute Lung Injury (pathology)</term>
<term>Animals</term>
<term>Anti-Inflammatory Agents (pharmacology)</term>
<term>Antibiotics, Antineoplastic (pharmacology)</term>
<term>Bleomycin (toxicity)</term>
<term>Bronchoalveolar Lavage Fluid (immunology)</term>
<term>Cytokines (blood)</term>
<term>Cytokines (drug effects)</term>
<term>Cytokines (metabolism)</term>
<term>Dexamethasone (pharmacology)</term>
<term>Disease Models, Animal</term>
<term>Hydroxyproline (analysis)</term>
<term>Lipopolysaccharides (immunology)</term>
<term>Pulmonary Fibrosis (etiology)</term>
<term>Pulmonary Fibrosis (immunology)</term>
<term>Pulmonary Fibrosis (pathology)</term>
<term>Rats</term>
<term>Rats, Wistar</term>
<term>STAT Transcription Factors (drug effects)</term>
<term>STAT Transcription Factors (immunology)</term>
<term>STAT Transcription Factors (metabolism)</term>
<term>Smad Proteins (drug effects)</term>
<term>Smad Proteins (immunology)</term>
<term>Smad Proteins (metabolism)</term>
<term>Th1 Cells (drug effects)</term>
<term>Th1 Cells (immunology)</term>
<term>Th1 Cells (metabolism)</term>
<term>Th2 Cells (drug effects)</term>
<term>Th2 Cells (immunology)</term>
<term>Th2 Cells (metabolism)</term>
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<term>Antibiotiques antinéoplasiques (pharmacologie)</term>
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<term>Cytokines ()</term>
<term>Cytokines (métabolisme)</term>
<term>Cytokines (sang)</term>
<term>Dexaméthasone (pharmacologie)</term>
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<front><div type="abstract" xml:lang="en">Based on the common characteristic of severe acute respiratory syndrome (SARS) and highly pathogenic avian influenza and the mechanism of inflammation and fibrosis, it is speculated that there should exist a fundamental pathological rule that severe acute lung injury (ALI)-induced rapid pulmonary fibrosis is caused by various etiological factors, such as SARS coronavirus, H5N1-virus, or other unknown factors, and also by lipopolysaccharide (LPS), the most common etiological factor. The investigation employed intratracheally, and intraperitoneally and intratracheally applied LPS three-hit regimen, compared with bleomycin-induced chronic pulmonary fibrosis. Inflammatory damage and fibrosis were evaluated, and the molecular mechanism was analyzed according to Th1/Th2 balance, Sma- and MAD-related proteins (Smads) and signal transducer and activator of transcriptions (STATs) expression. The results suggested that rapid pulmonary fibrosis could be induced by ALI via LPS three-hits. The period from 3-7 days in the LPS group was the first rapid pulmonary fibrosis stage, whereas the second fast fibrosis stage occurred on days 14-21. Th2 cell polarization, Smad4 and Smad7 should be the crucial molecular mechanism of ALI-induced rapid fibrosis. The investigation was not only performed to establish a new rapid pulmonary fibrosis model, but also to provide the elicitation for mechanism of ALI changed into the rapid pulmonary fibrosis.</div>
</front>
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