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Inflammation Itself Signals A Halt To Mounting Immune Responses

  July, 2 2001 2:20
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Conflict resolution in inflammation

Acute inflammation, as can occur after wounding or infection, proceeds along a precise time-course during which the immune system is activated, commits to battle at the site of tissue damage, and then, somewhat amazingly, disarms once the immediate danger is over. Turning off these inflammatory responses is key to limiting collateral damage to the surrounding tissues. But how does this occur? A paper in the July issue of Nature Immunology (Vol. 2, No. 7, pages 612-619) suggests that inflammation itself signals a halt to mounting immune responses.

Researchers from Charles Serhan’s laboratory in Boston have shown that a class of lipids, called eicosanoids, appears at distinct phases of an inflammatory response. First, leukotrienes, which recruit and activate leukocytes, are generated at the site of injury. These agents trigger the expression of an enzyme called cyclooxygenase 2 (COX-2), which maintains many of the facets of inflammation and is the target of several anti-inflammatory agents used therapeutically. However, COX-2 also generates prostaglandin E2 (PGE2), another eicosanoid that signals retreat. Lipoxin synthesis is also activated by the inflammatory leukotrienes. These molecules, which appear late in the response, halt further recruitment of leukocytes into the wounded tissues and terminate elaboration of inflammatory signals. Thus, resolution of inflammation is signaled at the onset of the response.

This paper was featured, in a beautiful illustration featuring a rendition of the vasculature system superimposed with a model of a lipoxin, as the Cover of the July issue of Nature Immunology.

Charles N. Serhan
Harvard Medical School
Brigham and Women's Hospital
Department of Anesthesiology
Center for Experimental Therapeutics and Reperfusion Injury
75 Francis Street
Boston, MA 02115
Tel: (+1) 617-732-8822
Fax: (+1) 617-278-6957

(C) Nature Immunology press release.

Message posted by: Trevor M. D'Souza

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