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JCI online early table of contents: Jan. 4, 2011
Date:1/4/2011

g/articles/view/41931?key=298a95f51658bfbedd1b">http://www.jci.org/articles/view/41931?key=298a95f51658bfbedd1b


INFLAMMATION: New point of control for inflammation: the soluble factor leukotriene B4

Inappropriate inflammation is central to many diseases, including asthma, autoimmune disease, and atherosclerosis (often known as hardening of the arteries). Signaling through several sets of cell surface molecules on immune cells known as macrophages is a key driver of inflammation. In particular, signaling through proteins that rely on the adaptor protein MyD88. A team of researchers, led by Marc Peters-Golden and Carlos Serezani, at the University of Michigan Health System, Ann Arbor, has now shown that mouse macrophage inflammatory responses dependent on MyD88 are reduced in the absence of signals triggered by the molecule leukotriene B4 (LTB4). These data have clinical importance, as they suggest that inhibitors of LTB4 generation and or antagonists of the molecule to which it binds might provide a new therapeutic approach to dampening inflammatory disease.

TITLE: Leukotriene B4 amplifies NF-kappa-B activation in mouse macrophages by reducing SOCS1 inhibition of MyD88 expression

AUTHOR CONTACT:
Marc Peters-Golden
University of Michigan Health System, Ann Arbor, Michigan, USA.
Phone: 734.763.9077; Fax: 734.764.4556; E-mail: petersm@umich.edu.

Carlos H. Serezani
University of Michigan Health System, Ann Arbor, Michigan, USA.
Phone: 734.615.5523; Fax: 734.764.4556; E-mail: cserezan@med.umich.edu.

View this article at: http://www.jci.org/articles/view/43302?key=122f690f1a4619d60b0d


NEUROBIOLOGY: New link between distinct neurological diseases

Amyotrophic lateral sclerosis (ALS;
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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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