NDLI: Annexin A1 regulates intestinal mucosal injury, inflammation, and repair.

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Annexin A1 regulates intestinal mucosal injury, inflammation, and repair.

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Year: 2008 Volume: 181 Issue: 6

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Annexin A1 regulates intestinal mucosal injury, inflammation, and repair.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Flower, Roderick J. Laukoetter, Mike G. Lee, Winston Y. Koch, Stefan Severson, Eric A. Babbin, Brian A. Nusrat, Asma Parkos, Charles A. Perretti, Mauro Nava, Porfirio Peatman, Eric Capaldo, Christopher T.
Description	Country affiliation: United States Author Affiliation: Babbin BA ( Epithelial Pathobiology Research Unit, Department of Pathology, Emory University, Atlanta, GA 30322, USA.)
Abstract	During mucosal inflammation, a complex array of proinflammatory and protective mechanisms regulates inflammation and severity of injury. Secretion of anti-inflammatory mediators is a mechanism that is critical in controlling inflammatory responses and promoting epithelial restitution and barrier recovery. AnxA1 is a potent anti-inflammatory protein that has been implicated to play a critical immune regulatory role in models of inflammation. Although AnxA1 has been shown to be secreted in intestinal mucosal tissues during inflammation, its potential role in modulating the injury/inflammatory response is not understood. In this study, we demonstrate that AnxA1-deficient animals exhibit increased susceptibility to dextran sulfate sodium (DSS)-induced colitis with greater clinical morbidity and histopathologic mucosal injury. Furthermore, impaired recovery following withdrawal of DSS administration was observed in AnxA1 (-/-) animals compared with wild-type (WT) control mice that was independent of inflammatory cell infiltration. Since AnxA1 exerts its anti-inflammatory properties through stimulation of ALX/FPRL-1, we explored the role of this receptor-ligand interaction in regulating DSS-induced colitis. Interestingly, treatment with an ALX/FPRL-1 agonist, 15-epi-lipoxin A4 reversed the enhanced sensitivity of AnxA1 (-/-) mice to DSS colitis. In contrast, 15-epi-lipoxin A4 did not significantly improve the severity of disease in WT animals. Additionally, differential expression of ALX/FPLR-1 in control and DSS-treated WT and AnxA1-deficient animals suggested a potential role for AnxA1 in regulating ALX/FPRL-1 expression under pathophysiological conditions. Together, these results support a role of endogenous AnxA1 in the protective and reparative properties of the intestinal mucosal epithelium.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	7
Volume Number	181
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2008-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Annexin A1 Physiology Inflammation Mediators Intestinal Mucosa Metabolism Pathology Wound Healing Immunology Animals Biosynthesis Deficiency Genetics Colitis Chemically Induced Dextran Sulfate Toxicity Genetic Predisposition To Disease Drug Effects Mice Mice, Inbred Balb C Mice, Knockout Severity Of Illness Index Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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