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Annexin A1 regulates intestinal mucosal injury, inflammation, and repair
Epithelial Pathobiology Research Unit, Department of Pathology, Emory University, Atlanta, GA, USA.
Department of General Surgery, University of Muenster, Muenster, Germany.
Epithelial Pathobiology Research Unit, Department of Pathology, Emory University, Atlanta, GA, USA.
Epithelial Pathobiology Research Unit, Department of Pathology, Emory University, Atlanta, GA, USA.
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2008 (engelsk)Inngår i: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, J Immunol, Vol. 181, nr 7, s. 5035-5044Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

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.

sted, utgiver, år, opplag, sider
Bethesda, United States: American Association of Immunologists , 2008. Vol. 181, nr 7, s. 5035-5044
Emneord [en]
Animals, Annexin A1/biosynthesis/deficiency/genetics/*physiology, Colitis/chemically induced/metabolism/pathology, Dextran Sulfate/toxicity, Female, Genetic Predisposition to Disease, Inflammation Mediators/metabolism/*physiology, Intestinal Mucosa/drug effects/*metabolism/*pathology, Mice, Mice, Inbred BALB C, Mice, Knockout, Severity of Illness Index, Wound Healing/drug effects/*immunology
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Identifikatorer
URN: urn:nbn:se:liu:diva-141649DOI: 10.4049/jimmunol.181.7.5035ISI: 000259755700067PubMedID: 18802107Scopus ID: 2-s2.0-58149279844ISBN: 1550-6606 (Electronic) 0022-1767 (Linking) OAI: oai:DiVA.org:liu-141649DiVA, id: diva2:1149720
Merknad

Babbin, Brian A Laukoetter, Mike G Nava, Porfirio Koch, Stefan Lee, Winston Y Capaldo, Christopher T Peatman, Eric Severson, Eric A Flower, Roderick J Perretti, Mauro Parkos, Charles A Nusrat, Asma eng K08 DK074706/DK/NIDDK NIH HHS/ R01 DK059888-09/DK/NIDDK NIH HHS/ R01 DK061379-08/DK/NIDDK NIH HHS/ R29 DK055679/DK/NIDDK NIH HHS/ T32 GM008169/GM/NIGMS NIH HHS/ K08 DK074706-02/DK/NIDDK NIH HHS/ R01-DK61379/DK/NIDDK NIH HHS/ DK 55679/DK/NIDDK NIH HHS/ DK64399/DK/NIDDK NIH HHS/ R01 DK072564/DK/NIDDK NIH HHS/ T32 DK007771-09/DK/NIDDK NIH HHS/ R24 DK064399/DK/NIDDK NIH HHS/ R01 DK055679-11A1/DK/NIDDK NIH HHS/ R24 DK064399-019003/DK/NIDDK NIH HHS/ R01 DK055679/DK/NIDDK NIH HHS/ DK 59888/DK/NIDDK NIH HHS/ R01 DK061379/DK/NIDDK NIH HHS/ R01-DK72564/DK/NIDDK NIH HHS/ T32 DK007771/DK/NIDDK NIH HHS/ R01 DK059888/DK/NIDDK NIH HHS/ K08 DK074706-01/DK/NIDDK NIH HHS/ R01 DK072564-15/DK/NIDDK NIH HHS/ Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't 2008/09/20 09:00 J Immunol. 2008 Oct 1;181(7):5035-44.

Tilgjengelig fra: 2017-10-16 Laget: 2017-10-16 Sist oppdatert: 2018-01-13bibliografisk kontrollert

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