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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Annexin-A1 peptide down-regulates the leukocyte recruitment and up-regulates interleukin-10 release into lung after intestinal ischemia-reperfusion in mice

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Author(s):
Guido, Bruna Candido [1] ; Zanatelli, Marianna [1] ; Tavares-de-Lima, Wothan [2] ; Oliani, Sonia Maria [1] ; Damazo, Amilcar Sabino [3]
Total Authors: 5
Affiliation:
[1] Sao Paulo State Univ UNESP, Dept Biol, Inst Biosci Letras & Ciencias Exatas IBILCE, BR-15054000 Sao Jose Do Rio Preto, SP - Brazil
[2] Univ Sao Paulo, Dept Pharmacol, Inst Biomed Sci ICB, BR-05508900 Sao Paulo - Brazil
[3] Fed Univ Mato Grosso UFMT, Fac Med FM, Dept Basic Sci Hlth, BR-78060900 Mato Grosso, MT - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Journal of Inflammation-London; v. 10, MAR 13 2013.
Web of Science Citations: 16
Abstract

Background: Intestinal ischemia/reperfusion (IR) injury is a serious and triggering event in the development of remote organ dysfunction, from which the lung is the main target. This condition is characterized by intense neutrophil recruitment, increased microvascular permeability. Intestinal IR is also responsible for induction of adult respiratory distress syndrome, the most serious and life-threatening form of acute lung injury. The purpose of this study was to investigate the effect of annexin-A1 protein as an endogenous regulator of the organ remote injury induced by intestinal ischemia/reperfusion. Male C57bl/6 mice were subjected to intestinal ischemia, induced by 45 min occlusion of the superior mesenteric artery, followed by reperfusion. Results: The intestinal ischemia/reperfusion evoked a high intensity lung inflammation as indicated by the number of neutrophils as compared to control group. Treatment with annexin-A1 peptidomimetic Ac2-26, reduced the number of neutrophils in the lung tissue and increased its number in the blood vessels, which suggests a regulatory effect of the peptide Ac2-26 in the neutrophil migration. Moreover, the peptide Ac2-26 treatment was associated with higher levels of plasma IL-10. Conclusion: Our data suggest that the annexin-A1 peptidomimetic Ac2-26 treatment has a regulatory and protective effect in the intestinal ischemia/reperfusion by attenuation of the leukocyte migration to the lung and induction of the anti-inflammatory cytokine IL-10 release into the plasma. The anti-inflammatory action of annexin-A1 and its peptidomimetic described here may serve as a basis for future therapeutic approach in mitigating inflammatory processes due to intestinal ischemia/reperfusion. (AU)

FAPESP's process: 07/01874-3 - Analysis of annexin-A1 protective role during splanchnic trauma induced by intestinal ischaemia/reperfusion
Grantee:Bruna Cândido Guido
Support Opportunities: Scholarships in Brazil - Scientific Initiation