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Role of IL-1B in TLR4-mediated MCP-1expression: renal sepsis

 

"Research Article"

American Journal of BioMedicine  Volume 3, Issue 1, pages 22-31, January 2015


Grace Hullmann; Michael A. Azfer; Jordan Hensley; Albertine Bergese; Jack Lefer

Abstract

Interleukin-1 (IL-1) family is a critical mediator of immune response to sepsis with two agonists (IL-1α and IL-1β) and one antagonist (IL-1 receptor antagonist: IL-1ra). Excessive IL-1 production is directly linked to the development of shock, multi-organ system failure, and death in patients and animals with sepsis, systemic inflammatory response syndrome, and septic shock. Further, recent reports have indicated that IL-1[beta] is excessively released into the circulation during renal sepsis. The ojective of this study is to investigate the effective role of IL-1β in mechanism of TLR4-induces renal sepsis. LPS administration induces systemic inflammation in wild type mice that mimics many of the initial clinical features of sepsis, including increases in proinflammatory cytokines. renal function was assessed and Chemokines and cytokines in plasma and renal tissue were analyzed by enzyme-linked immunosorbent assay (ELISA). Mononuclear cells in the myocardium were examined using immunofluorescence staining.IL-1β and other proinflammatory cytokines were measured. The WT mice have enhanced inflammatory responses to sepsis that lead to exaggerated renal functional reduction. MCP-1 promotes renal mononuclear cell accumulation, These results demonstrate that IL-1β plays a detrimental role in the development of renal sepsis in this murine model, suggesting that it may be applicable to clinical situations, such as trauma, shock and renal transplantation.

Keywords: Renal sepsis; IL-1β; Cytokines; MCP-1


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