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JCI online early table of contents: Jan. 9, 2012
Date:1/9/2012

attack by studying a mouse model of allergic asthma. Specifically, the team found that the protein complex alpha-v-beta-6 integrin modulates, via its effects on the soluble protein TGF-beta, the expression of mediators of airway narrowing known as mast cell proteases. As mice lacking alpha-v-beta-6 integrin were protected from exaggerated airway narrowing in their model, Sheppard and colleagues suggest that targeting this pathway could provide a new approach to treating allergic asthma.

TITLE: The alpha-v-beta-6 integrin modulates airway hyperresponsiveness in mice by regulating intraepithelial mast cells

AUTHOR CONTACT:
Dean Sheppard
University of California, San Francisco, San Francisco, California, USA.
Phone: 415-514-4269, Fax: 415-514-4278; E-mail: Dean.Sheppard@ucsf.edu.

View this article at:
http://www.jci.org/articles/view/58815?key=c0fbf3396c0256802880

BACTERIOLOGY: Making life inHUSpitable for bacterial toxins by targeting the CXCR4/SDF-1 interaction

Hemolytic uremic syndrome (HUS) is a potentially life-threatening condition. It often occurs after gastrointestinal infection with the bacterium Escherichia coli O157:H7. The bacterium releases toxins known as Shiga toxins (Stx), which cause the symptoms of HUS. A team of researchers led by Philip Marsden, at the University of Toronto, Toronto, has now defined a new molecular pathway by which Stx cause HUS. Specifically, the team identified a role for the soluble factor SDF-1 and the cell-surface proteins to which it binds (CXCR4 and CXCR7). Importantly, inhibition of the CXCR4/SDF-1 interaction decreased organ injury and improved survival in a mouse model of Stx-mediated disease, and levels of SDF-1 in the blood of children infected with Escherichia coli O157:H7 were elevated in those that developed HUS. Marsden and co
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Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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