dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorGuido, Bruna Candido
dc.creatorZanatelli, Marianna
dc.creatorTavares-De-Lima, Wothan
dc.creatorOliani, Sonia Maria
dc.creatorDamazo, Amílcar Sabino
dc.date2014-05-27T11:28:40Z
dc.date2016-10-25T18:45:36Z
dc.date2014-05-27T11:28:40Z
dc.date2016-10-25T18:45:36Z
dc.date2013-03-15
dc.date.accessioned2017-04-06T02:16:48Z
dc.date.available2017-04-06T02:16:48Z
dc.identifierJournal of Inflammation (United Kingdom), v. 10, n. 1, 2013.
dc.identifier1476-9255
dc.identifierhttp://hdl.handle.net/11449/74840
dc.identifierhttp://acervodigital.unesp.br/handle/11449/74840
dc.identifier10.1186/1476-9255-10-10
dc.identifierWOS:000316747500001
dc.identifier2-s2.0-84874805360.pdf
dc.identifier2-s2.0-84874805360
dc.identifierhttp://dx.doi.org/10.1186/1476-9255-10-10
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/895599
dc.descriptionBackground: 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. © 2013 Guido et al.; licensee BioMed Central Ltd.
dc.languageeng
dc.relationJournal of Inflammation (United Kingdom)
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAnnexin-A1
dc.subjectInterleukin-10 (IL-10)
dc.subjectLung
dc.subjectMacrophage
dc.subjectNeutrophil
dc.subjectinterleukin 10
dc.subjectlipocortin 1
dc.subjecttumor necrosis factor alpha
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectcontrolled study
dc.subjectcytokine production
dc.subjectdown regulation
dc.subjectintestine ischemia
dc.subjectleukocyte migration
dc.subjectlung blood vessel
dc.subjectlung injury
dc.subjectlung parenchyma
dc.subjectmale
dc.subjectmouse
dc.subjectneutrophil
dc.subjectnonhuman
dc.subjectpeptidomics
dc.subjectpneumonia
dc.subjectprotein blood level
dc.subjectprotein expression
dc.subjectprotein function
dc.subjectprotein secretion
dc.subjectreperfusion injury
dc.subjectsuperior mesenteric artery
dc.subjectupregulation
dc.subjectMus
dc.titleAnnexin-A1 peptide down-regulates the leukocyte recruitment and up-regulates interleukin-10 release into lung after intestinal ischemia-reperfusion in mice
dc.typeOtro


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