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JCI table of contents: Nov. 8, 2007
Date:11/8/2007

ignaling cascade downstream of IL-1R1 and TLRs, exhibited decreased lung inflammation and fibrosis compared with normal mice. Consistent with a key role for IL-1R1 signaling in mediating bleomycin-induced lung damage, specific blockade of IL-1R1 by IL-1 receptor antagonist dramatically reduced bleomycin-induced inflammation in normal mice. Further analysis revealed that a protein known as ASC, which is part of a multiprotein complex known as the inflammasome, was required for the production of IL-1-beta by the lung in response to exposure to bleomycin. These data indicate a requirement for IL-1, the inflammasome, and IL-1R1/MyD88 signaling in bleomycin-induced lung damage, and led the authors to suggest that targeting this pathway might provide a new approach to treating chronic lung inflammation and fibrosis, such as occurs in individuals with IPF.

TITLE: IL-1R1/MyD88 signaling and the inflammasome are essential in pulmonary inflammation and fibrosis in mice

AUTHOR CONTACT:
Isabelle Couillin
University of Orleans and CNRS, Orleans, France.
Phone: 33-238-25-54-39; Fax: 33-238-25-79-79; E-mail: couillin@cnrs-orleans.fr.

MEDIA CONTACT:
Martine Hasler
Head of Press Office
Centre National De La Reserche Scientifique, France
Phone: 33-1-44-96-46-35; Email: martine.hasler@cnrs-dir.fr.

View the PDF of this article at: https://www.the-jci.org/article.php?id=32285


NEPHROLOGY: A bone to pick with the parathyroid

A careful balance of mineral levels in the blood is necessary for life. A feedback loop between levels of phosphate, vitamin D, and the bone-derived hormone FGF23 helps to maintain this balance. FGF23 has been shown to bind cells in the kidneys, where it blocks the removal of phosphates from the blood and decrease
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Journal of Clinical Investigation
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