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

Please wait, while we are loading the content...

Year: 2017 Volume: 23

Year: 2016 Volume: 22

Year: 2015 Volume: 21

Year: 2014 Volume: 20

Year: 2013 Volume: 19

Year: 2012 Volume: 18

Year: 2011 Volume: 17

Year: 2010 Volume: 16

Year: 2009 Volume: 15

Year: 2009 Volume: 15 Issue: 4

Year: 2009 Volume: 15 Issue: 3

Differential modulation of NF-kappaB-mediated pro-inflammatory response in human intestinal epithelial cells by cheY homologues of Vibrio cholerae.

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

Activation of Toll-like receptors 2 and 4 in Aspergillus fumigatus keratitis.

Activation of peroxisome proliferator-activated receptor-gamma potentiates pro-inflammatory cytokine production, and adrenal and somatotropic changes of weaned pigs after Escherichia coli lipopolysaccharide challenge.

Review: Immunity mechanisms in crustaceans.

Year: 2009 Volume: 15 Issue: 2

Year: 2008 Volume: 14

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

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Li, Hui Du, Shaohui Yang, Lina Chen, Yangyan Huang, Wei Zhang, Rong Cui, Yinghai Yang, Jun Chen, Dongfeng Li, Yiwei Zhang, Saixia Zhou, Jianhong Wei, Zhijun Yao, Zhibin
Description	Author Affiliation: Li H ( Department of Anatomy, Guangzhou University of Chinese Medicine, Guangzhou, People's Republic of China.)
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.
File Format	HTM / HTML
ISSN	17534259
Issue Number	3
Volume Number	15
e-ISSN	17534267
Journal	Innate Immunity
Language	English
Publisher	Sage Publications
Publisher Date	2009-06-01
Publisher Place	United States
Access Restriction	Subscribed
Subject Keyword	Discipline Allergy and Immunology Discipline Bacteriology Acute Lung Injury Immunology Lipopolysaccharides Pulmonary Fibrosis Chemically Induced Complications Pathology Animals Anti-inflammatory Agents Pharmacology Antibiotics, Antineoplastic Bleomycin Toxicity Bronchoalveolar Lavage Fluid Cytokines Blood Drug Effects Metabolism Dexamethasone Disease Models, Animal Hydroxyproline Analysis Etiology Rats Rats, Wistar Stat Transcription Factors Smad Proteins Th1 Cells Th2 Cells Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Infectious Diseases Cell Biology Molecular Biology Immunology Microbiology

Central Library (ISO-9001:2015 Certified)
Indian Institute of Technology Kharagpur
Kharagpur, West Bengal, India | PIN - 721302

See location in the Map
03222 282435
Mail: support@ndl.gov.in

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in