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Please use this identifier to cite or link to this item: http://hdl.handle.net/1807/8199

Title: The balance between the production of tumor necrosis factor-α and interleukin-10 determines tissue injury and lethality during intestinal ischemia and reperfusion
Authors: Souza, Danielle G.
Teixeira, Mauro M.
Keywords: inflammatory response - tumor necrosis factor-α - interleukin-10 - neutrophil - ischemia and reperfusion
Issue Date: 31-Dec-2005
Publisher: Fundação Oswaldo Cruz, Fiocruz
Citation: Memórias do Instituto Oswaldo Cruz (ISSN: 1678-8060) Vol 100 Num s1
Abstract: A major goal in the treatment of acute ischemia of a vascular territory is to restore blood flow to normal values, i.e. to "reperfuse" the ischemic vascular bed. However, reperfusion of ischemic tissues is associated with local and systemic leukocyte activation and trafficking, endothelial barrier dysfunction in postcapillary venules, enhanced production of inflammatory mediators and great lethality. This phenomenon has been referred to as "reperfusion injury" and several studies demonstrated that injury is dependent on neutrophil recruitment. Furthermore, ischemia and reperfusion injury is associated with the coordinated activation of a series of cytokines and adhesion molecules. Among the mediators of the inflammatory cascade released, TNF-α appears to play an essential role for the reperfusion-associated injury. On the other hand, the release of IL-10 modulates pro-inflammatory cytokine production and reperfusion-associated tissue injury. IL-1β, PAF and bradykinin are mediators involved in ischemia and reperfusion injury by regulating the balance between TNF-α and IL-10 production. Strategies that enhance IL-10 and/or prevent TNF-α concentration may be useful as therapeutic adjuvants in the treatment of the tissue injury that follows ischemia and reperfusion.
URI: http://hdl.handle.net/1807/8199
Other Identifiers: http://www.bioline.org.br/abstract?id=oc05028
Rights: Copyright 2005 - Instituto Oswaldo Cruz - Fiocruz.
Appears in Collections:Bioline International Legacy Collection

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