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  3. Clinical Laboratory Sciences and Medical Biotechnology / 醫學檢驗暨生物技術學系所
  4. The bacterial metabolite 2,3-butanediol ameliorates endotoxin-induced acute lung injury in rats
 
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The bacterial metabolite 2,3-butanediol ameliorates endotoxin-induced acute lung injury in rats

Journal
Microbes and Infection
Journal Volume
9
Journal Issue
12-13
Pages
1402-1409
Date Issued
2007
Author(s)
Hsieh S.-C.
Lu C.-C.
Horng Y.-T.
Soo P.-C.
Chang Y.-L.
Tsai Y.-H.
Lin C.-S.
HSIN-CHIH LAI  
DOI
10.1016/j.micinf.2007.07.004
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/508255
Abstract
Widely identified in bacteria, yeasts and human beings, 2,3-butanediol has been studied for decades.This chemical reportedly functions as a neutralization agent to counteract lethal acidification by bacterial growth and as a signaling molecule involved in interactions among insects, and between bacteria and the plant host. While 2,3-butanediol is produced by many pathogenic bacterial species, its significance and effect on mammals remains basically uncharacterized. Herein, we show that gastric intubation of 2,3-butanediol in rats significantly ameliorates acute lung injury (ALI) and the inflammatory responses induced by the bacterial endotoxin lipopolysaccharide (LPS), with an efficacy comparable to that of the polyphenol compound resveratrol. Such effect was further demonstrated to occur via modulation of the NF-κB signaling pathway. These results indicate that bacterial metabolite, 2,3-butanediol has a negative regulatory effect on host innate immunity response, suggesting bacteria may use some metabolites for host immune evasion. ? 2007 Elsevier Masson SAS. All rights reserved.
Subjects
2,3-butanediol; Acute lung injury; Inflammation; LPS; NF-κB
SDGs

[SDGs]SDG3

Other Subjects
2,3 butanediol; bacterium lipopolysaccharide; endotoxin; immunoglobulin enhancer binding protein; polyphenol; resveratrol; acidification; acute lung injury; animal experiment; animal model; animal tissue; article; bacterial growth; bacterial infection; controlled study; disease model; host pathogen interaction; host resistance; inflammation; male; nonhuman; priority journal; rat; signal transduction; Sprague Dawley rat; Animals; Anti-Inflammatory Agents; Butylene Glycols; Endotoxins; Inflammation; Lipopolysaccharides; Lung; Male; NF-kappa B; Rats; Rats, Sprague-Dawley; Signal Transduction; Treatment Outcome; Bacteria (microorganisms); Hexapoda; Mammalia; Rattus
Type
journal article

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