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• W2543529510 abstract "Leptin is an adipose tissue-produced hormone/cytokine which inhibits food intake and lipid metabolism. It is highly expressed in obesity without appetite inhibition enhancement. Also regulates innate and adaptive immunity. It is known that leptin activates macrophages inducing the production of inflammatory mediators such as TNF-F061, IL-1, IL-6 and LTB4. Leptin regulates neutrophil functions in inflammatory responses. However, mechanisms by which leptin could induce neutrophils migration and activation are not elucidated, since they do not show the main functional leptin receptor, ObRb. In vitro studies are inconclusive about direct or indirect effects, while in vivo studies usually do not focus on leptin effects on neutrophil chemotaxis. This study aims to investigate leptin signaling involved in neutrophil migration. C57BL/6 and knockout TNFR1-/-, MIP-1F061-/-, 5-LO-/-, PI3KF067-/- male mice were stimulated with leptin ip for 1, 6 or 24 h for evaluation of neutrophil influx into peritoneal cavity and quantification of inflammatory mediators in the supernatant of peritoneal fluid and plasma. It was also performed treatments with rapamycin, for inhibition of mTOR, Zileuton and U-75302 for inhibition of LTB4 signaling, and anti-KC antibodies. Macrophages incubated with 20 nM leptin in vitro produce KC and TNF-F061, neutrophil recruitment mediators. In vivo, neutrophil migration induced by leptin is dependent on TNF-F061, KC and PI3KF067, and independent on 5-LO/LTB4, MIP-1F061 and mTORTo evaluate the effect of chronic hyperleptinemia in innate immunity, we established a murine model of diet induced obesity. The obese animals were fed with high fat diet with 60% calories from fat content, while the control diet had 10% of caloric content derived from fat. Obese animals showed hyperglycemia and hyperleptinemia. The fat diet predisposed the activation of peritoneal macrophages by leptin, increasing the lipid bodies formation. The levels of TNF-F061 in the supernatant of peritoneal fluid were higher in obese animals, not stimulated with leptin ip; leptin ip stimulus induced neutrophil recruitment in obese animals. Such events suggest that the high fat diet induced inflammatory background, which, however, did not affect the ability of leptin to induce neutrophil recruitment. These data suggest that leptin promotes neutrophils recruitment through the activation of macrophages and production of mediators. Furthermore, experimental obesity promotes subclinical activation of macrophages, without changing the recruitment of neutrophils. This thesis is expected to contribute to a better understanding of leptin role in the regulation of innate immune system" @default.
• W2543529510 created "2016-11-04" @default.
• W2543529510 creator A5079961855 @default.
• W2543529510 date "2012-01-01" @default.
• W2543529510 modified "2023-09-24" @default.
• W2543529510 title "Recrutamento de neutrófilos induzido por leptina em modelo murino de obesidade induzida por dieta" @default.
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