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.
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Authors | Hui Li, 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 Yao |
Journal | Innate immunity
(Innate Immun)
Vol. 15
Issue 3
Pg. 143-54
(Jun 2009)
ISSN: 1753-4259 [Print] United States |
PMID | 19474208
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Anti-Inflammatory Agents
- Antibiotics, Antineoplastic
- Cytokines
- Lipopolysaccharides
- STAT Transcription Factors
- Smad Proteins
- Bleomycin
- Dexamethasone
- Hydroxyproline
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Topics |
- Acute Lung Injury
(chemically induced, complications, immunology, pathology)
- Animals
- Anti-Inflammatory Agents
(pharmacology)
- Antibiotics, Antineoplastic
(pharmacology)
- Bleomycin
(toxicity)
- Bronchoalveolar Lavage Fluid
(immunology)
- Cytokines
(blood, drug effects, metabolism)
- Dexamethasone
(pharmacology)
- Disease Models, Animal
- Hydroxyproline
(analysis)
- Lipopolysaccharides
(immunology)
- Pulmonary Fibrosis
(etiology, immunology, pathology)
- Rats
- Rats, Wistar
- STAT Transcription Factors
(drug effects, immunology, metabolism)
- Smad Proteins
(drug effects, immunology, metabolism)
- Th1 Cells
(drug effects, immunology, metabolism)
- Th2 Cells
(drug effects, immunology, metabolism)
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