The balance between the production of tumor necrosis factor-alpha and interleukin-10 determines tissue injury and lethality during intestinal ischemia and reperfusion
Mem. Inst. Oswaldo Cruz
;
100(supl.1): 59-66, Mar. 2005. ilus
Artículo
en Inglés
| LILACS
| ID: lil-402177
RESUMO
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-alpha 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-1beta, PAF and bradykinin are mediators involved in ischemia and reperfusion injury by regulating the balance between TNF-alpha and IL-10 production. Strategies that enhance IL-10 and/or prevent TNF-alpha concentration may be useful as therapeutic adjuvants in the treatment of the tissue injury that follows ischemia and reperfusion.
Texto completo:
Disponible
Índice:
LILACS (Américas)
Asunto principal:
Daño por Reperfusión
/
Factor de Necrosis Tumoral alfa
/
Intestinos
/
Isquemia
/
Neutrófilos
Tipo de estudio:
Estudio de etiología
Límite:
Animales
/
Humanos
Idioma:
Inglés
Revista:
Mem. Inst. Oswaldo Cruz
Asunto de la revista:
Medicina Tropical
/
Parasitología
Año:
2005
Tipo del documento:
Artículo
País de afiliación:
Brasil
Institución/País de afiliación:
Universidade Federal de Minas Gerais/BR
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