JCI online early table of contents: Jan. 2, 2008

EDITOR'S PICK

Il-22 gene delivers the goods and decreases intestinal inflammation

There are two major types of inflammatory bowel disease (IBD), Crohn disease (CD) and ulcerative colitis (UC). Conflicting reports have indicated that the soluble factor IL-22 can have both IBD promoting and IBD controlling effects. But now, Atsushi Mizoguchi and colleagues at Massachusetts General Hospital, Boston, have established that IL-22 ameliorates disease in a mouse model of UC.

Expression of IL-22 is much higher in the intestines of individuals with CD than UC. To investigate the role of IL-22 in IBD, the authors used a new microinjection-based strategy to deliver the gene that makes IL-22 to the walls of the intestine of mice who suffer from an intestinal disease that models UC. Delivery of the Il-22 gene ameliorated local intestinal inflammation through enhanced mucus production. Consistent with this, when the same strategy was used to deliver a gene that makes a protein that neutralizes IL-22, IL-22–binding protein, to the walls of the intestines of normal mice it enhanced chemical-induced intestinal inflammation. The authors therefore suggest that individuals with UC might benefit from local delivery of the IL-22 gene to their intestines.

TITLE: IL-22 ameliorates intestinal inflammation in a mouse model of ulcerative colitis

AUTHOR CONTACT:
Atsushi Mizoguchi
Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Phone: (617) 726-2588; Fax: (617) 726-2365; E-mail: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=33194

EDITOR'S PICK

Epilepsy and brain pathology linked together by the protein ADK

The brain of individuals who suffer from epilepsy is characterized by astrogliosis, a brain pathology evidenced by a complex series of changes in the morphology and function of brain cells known as astrocytes. Little is known about how astrogliosis relates to the dysfunction of brain cells known as neurons in individuals with epilepsy, but filling in the blanks in our knowledge could lead to new possibilities for therapeutic intervention. A study using mice by Detlev Boison and colleagues at Legacy Clinical Research, Portland, has now identified the protein ADK in astrocytes as a molecular link between astrogliosis and neuronal dysfunction in epilepsy.