New Candidate To Prevent Inflammation

Main Category: GastroIntestinal / Gastroenterology
Article Date: 03 Jan 2009 - 0:00 PDT

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Dr. Sonia Oliani and colleagues at São Paulo State University have identified a potential new molecule that inhibits inflammation, receptor for formylated peptides-2 (FPR-2). These findings are presented in the January 2009 issue of The American Journal of Pathology.

Inflammation of the peritoneum is characterized by severe abdominal pain. This inflammation can be prevented by annexin A1, which inhibits the migration of inflammation-inducing white blood cells into the affected area.

In this study, Gastardelo et al examined the identities of the receptors responsible for the anti-inflammatory effects of annexin A1 in a mouse model of peritonitis. FPR family members had been previously shown to interact with annexin A1. Yet FPR-1-deficient mice, unlike annexin A1-null mice, did not have increased white blood cell recruitment. Instead, annexin A1 colocalized with another FPR family member, FPR-2.

The data by Gastardelo et al "provide in vivo evidence that endogenous annexin A1 is an essential mediator for homeostasis during the inflammatory process." They go on to propose "that these experimental findings may impact the development of novel therapeutics based on the anti-migratory actions of annexin A1."

Gastardelo TS, Damazo AS, Dalli J, Flower RJ, Perretti M, Oliani SM
"Functional and ultrastrutural analysis of annexin A1 and its receptor in extravasting neurophils during inflammation.
Am J Pathol 2009, 174:177-183

American Journal of Pathology, official journal of the American Society for Investigative Pathology, seeks to publish high-quality, original papers on the cellular and molecular biology of disease. The editors accept manuscripts that advance basic and translational knowledge of the pathogenesis, classification, diagnosis, and mechanisms of disease, without preference for a specific analytic method. High priority is given to studies on human disease and relevant experimental models using cellular, molecular, animal, biological, chemical, and immunological approaches in conjunction with morphology.

Source
Angela Colmone
American Journal of Pathology