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JCI Table of Contents, April 3, 2006

EF="https://www.the-jci.org/article.php?id=25422">https://www.the-jci.org/article.php?id=25422

ACCOMPANYING COMMENTARY:

TITLE: Pathomechanisms in rheumatoid arthritis --time for a string theory?

AUTHOR CONTACT: Cornelia M. Weyand
Emory University School of Medicine, Atlanta, Georgia, USA

Phone: (404) 727-7310; Fax: (404) 727-7371; E-mail: cweyand@emory.edu

View the PDF of this article at: https://www.the-jci.org/article.php?id=28300

IMMUNOLOGY

Protection from infection: how antioxidant signaling pathways can help

In a study appearing in the April issue of the Journal of Clinical Investigation, researcher Shyam Biswal and colleagues at the Johns Hopkins University in Baltimore report that mice that fail to express Nrf2, a protein involved in the expression of various antioxidant genes, are dramatically more susceptible to death following acute exposure to a bacterial cell wall sugar called LPS and to surgically-induced sepsis. The authors examined post-LPS-treatment lung inflammation in the mice and found that Nrf2-deficient animals had significantly higher levels of inflammatory cells called neutrophils, as well as higher levels of immune cells called macrophages, as soon as 6 hours after LPS exposure. The treatments also stimulated greater development of pulmonary edema, accompanied by elevated blood levels of the early-phase proinflammatory protein TNF-alpha in the Nrf2-deficient mice, compared to normal mice. Examination of antioxidants revealed that Nrf2-deficient mice expressed severely depressed levels of the tissue-protective enzyme glutathione, suggesting that Nrf2 plays a central role in controlling the body's proper immune response during infection. The authors note that these results provide insight into the immune system's response to sepsis and septic shock,
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Contact: Brooke Grindlinger
press_releases@the-jci.org
212-342-9006
Journal of Clinical Investigation
3-Apr-2006


Page: 1 2 3 4 5 6 7 8 9 10 11 12

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