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JCI early table of contents for Jan. 25, 2013
Date:1/25/2013

AUTHOR CONTACT:
Max S. Wicha
University of Michigan, Ann Arbor, MI, USA
Phone: 1-734-618-7324; E-mail: mwicha@med.umich.edu

View this article at: http://www.jci.org/articles/view/67460?key=37db186328102ebb8897


Researchers identify key mediators of sepsis-induced lung injury

Sepsis is an illness in which the body has a severe reaction to a bacterial infection. Bacterial toxins activate the immune system, causing widespread inflammation and increased blood calcium levels, oxidative stress, and inflammatory factors. This increased inflammation and immune activation can cause fatal organ damage, particularly in the lungs. The molecular mechanisms underlying this damage are unknown. In this issue of the Journal of Clinical Investigation, Madesh Muniswamy and colleagues at Temple University identified a signaling pathway that mediates lung injury during sepsis. Using a mouse model of sepsis-induced lung injury, Muniswamy and colleagues demonstrated that the proteins STIM1 and NOX2 drive the body's response to bacterial toxins, as mice lacking these proteins were not susceptible to lung injury. Additionally, treatment with a calcium channel blocker known as BTP2 halted sepsis-induced lung injury. These findings identify therapeutic targets that could be used to limit sepsis-induced lung injury.

TITLE:
Blockade of NOX2 and STIM1 signaling limits lipopolysaccharide-induced vascular inflammation

AUTHOR CONTACT:
Madesh Muniswamy
Temple University, Philadelphia, PA, USA
Phone: 2157075465; Fax: 2157077536; E-mail: madeshm@temple.edu

View this article at: http://www.jci.org/articles/view/65647?key=a0fec1e2ea29b7adbf2a
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Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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