| Literature DB >> 20601635 |
George D Leikauf1, Hannah Pope-Varsalona, Vincent J Concel, Pengyuan Liu, Kiflai Bein, Kelly A Brant, Richard A Dopico, Y Peter Di, An-Soo Jang, Maggie Dietsch, Mario Medvedovic, Qian Li, Louis J Vuga, Naftali Kaminski, Ming You, Daniel R Prows.
Abstract
Acute lung injury can be induced indirectly (e.g., sepsis) or directly (e.g., chlorine inhalation). Because treatment is still limited to supportive measures, mortality remains high ( approximately 74,500 deaths/yr). In the past, accidental (railroad derailments) and intentional (Iraq terrorism) chlorine exposures have led to deaths and hospitalizations from acute lung injury. To better understand the molecular events controlling chlorine-induced acute lung injury, we have developed a functional genomics approach using inbred mice strains. Various mouse strains were exposed to chlorine (45 ppm x 24 h) and survival was monitored. The most divergent strains varied by more than threefold in mean survival time, supporting the likelihood of an underlying genetic basis of susceptibility. These divergent strains are excellent models for additional genetic analysis to identify critical candidate genes controlling chlorine-induced acute lung injury. Gene-targeted mice then could be used to test the functional significance of susceptibility candidate genes, which could be valuable in revealing novel insights into the biology of acute lung injury.Entities:
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Year: 2010 PMID： 20601635 PMCID： PMC3136967 DOI： 10.1513/pats.201001-005SM
Source DB: PubMed Journal: Proc Am Thorac Soc ISSN： 1546-3222