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

Journal of Inflammation

Research

Amílcar Sabino Damazo¹  Sonia Maria Oliani²  Marianna Zanatelli²  Bruna Candido Guido²  Wothan Tavares-de-Lima³ 

[1] Department of Basic Science in Health; Faculty of Medicine (FM), Federal University of Mato Grosso (UFMT), 78060-900, Mato Grosso, MT, Brazil;Department of Biology; Institute of Biosciences, Letras e Ciências Exatas (IBILCE), São Paulo State University (UNESP), São José do Rio Preto, 15054-000, SP, Brazil;Department of Pharmacology, Institute of Biomedical Sciences (ICB), University of São Paulo (USP), 05508-900, São Paulo, Brazil;

关键词: Annexin-A1;    Lung;    Macrophage;    Neutrophil;    Interleukin-10 (IL-10);   

DOI  :  10.1186/1476-9255-10-10

 received in 2012-05-30, accepted in 2013-03-01,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundIntestinal 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.ResultsThe 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.ConclusionOur 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.

【 授权许可】

Unknown   
© Guido et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.