Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Sign In to gain access to subscriptions and/or personal tools.
Innate Immunity
This Article
Right arrow Full Text (PDF)
Right arrow Supplementary Material
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Hui Li
Right arrow Articles by Zhibin Yao
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hui Li,
Right arrow Articles by Zhibin Yao,
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Rapid pulmonary fibrosis induced by acute lung injury via a lipopolysaccharide three-hit regimen

Hui Li

Department of Anatomy, Guangzhou University of Chinese Medicine, Guangzhou, People's Republic of China

Shaohui Du

Department of Internal Medicine, Affiliated Shenzhen Hospital to Guangzhou University of Chinese Medicine, Shenzhen, People's Republic of China, dushaohui{at}tom.com

Lina Yang

Department of Internal Medicine, Affiliated Shenzhen Hospital to Guangzhou University of Chinese Medicine, Shenzhen, People's Republic of China

Yangyan Chen

Department of Internal Medicine, Affiliated Shenzhen Hospital to Guangzhou University of Chinese Medicine, Shenzhen, People's Republic of China

Wei Huang

Department of Internal Medicine, Affiliated Shenzhen Hospital to Guangzhou University of Chinese Medicine, Shenzhen, People's Republic of China

Rong Zhang

Department of Internal Medicine, Affiliated Shenzhen Hospital to Guangzhou University of Chinese Medicine, Shenzhen, People's Republic of China

Yinghai Cui

Department of Internal Medicine, Affiliated Shenzhen Hospital to Guangzhou University of Chinese Medicine, Shenzhen, People's Republic of China

Jun Yang

Department of Internal Medicine, Affiliated Shenzhen Hospital to Guangzhou University of Chinese Medicine, Shenzhen, People's Republic of China

Dongfeng Chen

Department of Anatomy, Guangzhou University of Chinese Medicine, Guangzhou, People's Republic of China

Yiwei Li

Department of Anatomy, Guangzhou University of Chinese Medicine, Guangzhou, People's Republic of China

Saixia Zhang

Department of Anatomy, Guangzhou University of Chinese Medicine, Guangzhou, People's Republic of China

Jianhong Zhou

Department of Anatomy, Guangzhou University of Chinese Medicine, Guangzhou, People's Republic of China

Zhijun Wei

Department of Internal Medicine, Affiliated Shenzhen Hospital to Guangzhou University of Chinese Medicine, Shenzhen, People's Republic of China

Zhibin Yao

Department of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, People's Republic of China

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.

Key Words: Acute lung injury • lipopolysaccharide • pulmonary fibrosis • signal transducer and activator of transcription • Sma- and MAD-related proteins

Innate Immunity, Vol. 15, No. 3, 143-154 (2009)
DOI: 10.1177/1753425908101509


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?