Rapid pulmonary fibrosis induced by acute lung injury via a lipopolysaccharide three-hit regimen.
Identifieur interne : 002A42 ( Main/Exploration ); précédent : 002A41; suivant : 002A43Rapid 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
Affiliations:
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Le document en format XML
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sortKey="Chen, Yangyan" sort="Chen, Yangyan" uniqKey="Chen Y" first="Yangyan" last="Chen">Yangyan Chen</name></author><author><name sortKey="Huang, Wei" sort="Huang, Wei" uniqKey="Huang W" first="Wei" last="Huang">Wei Huang</name></author><author><name sortKey="Zhang, Rong" sort="Zhang, Rong" uniqKey="Zhang R" first="Rong" last="Zhang">Rong Zhang</name></author><author><name sortKey="Cui, Yinghai" sort="Cui, Yinghai" uniqKey="Cui Y" first="Yinghai" last="Cui">Yinghai Cui</name></author><author><name sortKey="Yang, Jun" sort="Yang, Jun" uniqKey="Yang J" first="Jun" last="Yang">Jun Yang</name></author><author><name sortKey="Chen, Dongfeng" sort="Chen, Dongfeng" uniqKey="Chen D" first="Dongfeng" last="Chen">Dongfeng Chen</name></author><author><name sortKey="Li, Yiwei" sort="Li, Yiwei" uniqKey="Li Y" first="Yiwei" last="Li">Yiwei Li</name></author><author><name sortKey="Zhang, Saixia" sort="Zhang, Saixia" uniqKey="Zhang S" first="Saixia" last="Zhang">Saixia Zhang</name></author><author><name sortKey="Zhou, Jianhong" sort="Zhou, Jianhong" uniqKey="Zhou J" first="Jianhong" last="Zhou">Jianhong Zhou</name></author><author><name sortKey="Wei, Zhijun" sort="Wei, Zhijun" uniqKey="Wei Z" first="Zhijun" last="Wei">Zhijun Wei</name></author><author><name sortKey="Yao, Zhibin" sort="Yao, Zhibin" uniqKey="Yao Z" first="Zhibin" last="Yao">Zhibin Yao</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="RBID">pubmed:19474208</idno><idno type="pmid">19474208</idno><idno type="doi">10.1177/1753425908101509</idno><idno type="wicri:Area/PubMed/Corpus">001895</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001895</idno><idno type="wicri:Area/PubMed/Curation">001895</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001895</idno><idno type="wicri:Area/PubMed/Checkpoint">001808</idno><idno type="wicri:explorRef" 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University of Chinese Medicine, Guangzhou</wicri:regionArea><placeName><settlement type="city">Jiangmen</settlement><region type="province">Guangdong</region></placeName></affiliation></author><author><name sortKey="Du, Shaohui" sort="Du, Shaohui" uniqKey="Du S" first="Shaohui" last="Du">Shaohui Du</name></author><author><name sortKey="Yang, Lina" sort="Yang, Lina" uniqKey="Yang L" first="Lina" last="Yang">Lina Yang</name></author><author><name sortKey="Chen, Yangyan" sort="Chen, Yangyan" uniqKey="Chen Y" first="Yangyan" last="Chen">Yangyan Chen</name></author><author><name sortKey="Huang, Wei" sort="Huang, Wei" uniqKey="Huang W" first="Wei" last="Huang">Wei Huang</name></author><author><name sortKey="Zhang, Rong" sort="Zhang, Rong" uniqKey="Zhang R" first="Rong" last="Zhang">Rong Zhang</name></author><author><name sortKey="Cui, Yinghai" sort="Cui, Yinghai" uniqKey="Cui Y" first="Yinghai" last="Cui">Yinghai Cui</name></author><author><name sortKey="Yang, Jun" sort="Yang, Jun" uniqKey="Yang J" first="Jun" last="Yang">Jun Yang</name></author><author><name sortKey="Chen, Dongfeng" sort="Chen, Dongfeng" uniqKey="Chen D" first="Dongfeng" last="Chen">Dongfeng Chen</name></author><author><name sortKey="Li, Yiwei" sort="Li, Yiwei" uniqKey="Li Y" first="Yiwei" last="Li">Yiwei Li</name></author><author><name sortKey="Zhang, Saixia" sort="Zhang, Saixia" uniqKey="Zhang S" first="Saixia" last="Zhang">Saixia Zhang</name></author><author><name sortKey="Zhou, Jianhong" sort="Zhou, Jianhong" uniqKey="Zhou J" first="Jianhong" last="Zhou">Jianhong Zhou</name></author><author><name sortKey="Wei, Zhijun" sort="Wei, Zhijun" uniqKey="Wei Z" first="Zhijun" last="Wei">Zhijun Wei</name></author><author><name sortKey="Yao, Zhibin" sort="Yao, Zhibin" uniqKey="Yao Z" first="Zhibin" last="Yao">Zhibin Yao</name></author></analytic><series><title level="j">Innate immunity</title><idno type="ISSN">1753-4259</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Lung Injury (chemically induced)</term><term>Acute Lung Injury (complications)</term><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></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Anti-inflammatoires (pharmacologie)</term><term>Antibiotiques antinéoplasiques (pharmacologie)</term><term>Bléomycine (toxicité)</term><term>Cytokines ()</term><term>Cytokines (métabolisme)</term><term>Cytokines (sang)</term><term>Dexaméthasone (pharmacologie)</term><term>Facteurs de transcription STAT ()</term><term>Facteurs de transcription STAT (immunologie)</term><term>Facteurs de transcription STAT (métabolisme)</term><term>Fibrose pulmonaire (anatomopathologie)</term><term>Fibrose pulmonaire (immunologie)</term><term>Fibrose pulmonaire (étiologie)</term><term>Hydroxyproline (analyse)</term><term>Lipopolysaccharides (immunologie)</term><term>Liquide de lavage bronchoalvéolaire (immunologie)</term><term>Lymphocytes auxiliaires Th1 ()</term><term>Lymphocytes auxiliaires Th1 (immunologie)</term><term>Lymphocytes auxiliaires Th1 (métabolisme)</term><term>Lymphocytes auxiliaires Th2 ()</term><term>Lymphocytes auxiliaires Th2 (immunologie)</term><term>Lymphocytes auxiliaires Th2 (métabolisme)</term><term>Lésion pulmonaire aigüe ()</term><term>Lésion pulmonaire aigüe (anatomopathologie)</term><term>Lésion pulmonaire aigüe (immunologie)</term><term>Modèles animaux de maladie humaine</term><term>Protéines Smad ()</term><term>Protéines Smad (immunologie)</term><term>Protéines Smad (métabolisme)</term><term>Rat Wistar</term><term>Rats</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Hydroxyproline</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Cytokines</term><term>STAT Transcription Factors</term><term>Smad Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Lipopolysaccharides</term><term>STAT Transcription Factors</term><term>Smad Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>STAT Transcription Factors</term><term>Smad Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents</term><term>Antibiotics, Antineoplastic</term><term>Dexamethasone</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>Hydroxyproline</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Fibrose pulmonaire</term><term>Lésion pulmonaire aigüe</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Acute Lung Injury</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Acute Lung Injury</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Th1 Cells</term><term>Th2 Cells</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Pulmonary Fibrosis</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Facteurs de transcription STAT</term><term>Fibrose pulmonaire</term><term>Lipopolysaccharides</term><term>Liquide de lavage bronchoalvéolaire</term><term>Lymphocytes auxiliaires Th1</term><term>Lymphocytes auxiliaires Th2</term><term>Lésion pulmonaire aigüe</term><term>Protéines Smad</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Acute Lung Injury</term><term>Bronchoalveolar Lavage Fluid</term><term>Pulmonary Fibrosis</term><term>Th1 Cells</term><term>Th2 Cells</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Th1 Cells</term><term>Th2 Cells</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term><term>Facteurs de transcription STAT</term><term>Lymphocytes auxiliaires Th1</term><term>Lymphocytes auxiliaires Th2</term><term>Protéines Smad</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Acute Lung Injury</term><term>Pulmonary Fibrosis</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anti-inflammatoires</term><term>Antibiotiques antinéoplasiques</term><term>Dexaméthasone</term></keywords><keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Cytokines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Bleomycin</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Bléomycine</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Fibrose pulmonaire</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Rats</term><term>Rats, Wistar</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cytokines</term><term>Facteurs de transcription STAT</term><term>Lymphocytes auxiliaires Th1</term><term>Lymphocytes auxiliaires Th2</term><term>Lésion pulmonaire aigüe</term><term>Modèles animaux de maladie humaine</term><term>Protéines Smad</term><term>Rat Wistar</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><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></TEI><affiliations><list><country><li>République populaire de Chine</li></country><region><li>Guangdong</li></region><settlement><li>Jiangmen</li></settlement></list><tree><noCountry><name sortKey="Chen, Dongfeng" sort="Chen, Dongfeng" uniqKey="Chen D" first="Dongfeng" last="Chen">Dongfeng Chen</name><name sortKey="Chen, Yangyan" sort="Chen, Yangyan" uniqKey="Chen Y" first="Yangyan" last="Chen">Yangyan Chen</name><name sortKey="Cui, Yinghai" sort="Cui, Yinghai" uniqKey="Cui Y" first="Yinghai" last="Cui">Yinghai Cui</name><name sortKey="Du, Shaohui" sort="Du, Shaohui" uniqKey="Du S" first="Shaohui" last="Du">Shaohui Du</name><name sortKey="Huang, Wei" sort="Huang, Wei" uniqKey="Huang W" first="Wei" last="Huang">Wei Huang</name><name sortKey="Li, Yiwei" sort="Li, Yiwei" uniqKey="Li Y" first="Yiwei" last="Li">Yiwei Li</name><name sortKey="Wei, Zhijun" sort="Wei, Zhijun" uniqKey="Wei Z" first="Zhijun" last="Wei">Zhijun Wei</name><name sortKey="Yang, Jun" sort="Yang, Jun" uniqKey="Yang J" first="Jun" last="Yang">Jun Yang</name><name sortKey="Yang, Lina" sort="Yang, Lina" uniqKey="Yang L" first="Lina" last="Yang">Lina Yang</name><name sortKey="Yao, Zhibin" sort="Yao, Zhibin" uniqKey="Yao Z" first="Zhibin" last="Yao">Zhibin Yao</name><name sortKey="Zhang, Rong" sort="Zhang, Rong" uniqKey="Zhang R" first="Rong" last="Zhang">Rong Zhang</name><name sortKey="Zhang, Saixia" sort="Zhang, Saixia" uniqKey="Zhang S" first="Saixia" last="Zhang">Saixia Zhang</name><name sortKey="Zhou, Jianhong" sort="Zhou, Jianhong" uniqKey="Zhou J" first="Jianhong" last="Zhou">Jianhong Zhou</name></noCountry><country name="République populaire de Chine"><region name="Guangdong"><name sortKey="Li, Hui" sort="Li, Hui" uniqKey="Li H" first="Hui" last="Li">Hui Li</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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