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MyD88: a modulator of inflammatory and metabolic profile in experimental obesity.

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Angela Castoldi
Total Authors: 1
Document type: Doctoral Thesis
Press: São Paulo.
Institution: Universidade de São Paulo (USP). Instituto de Ciências Biomédicas
Defense date:
Examining board members:
Niels Olsen Saraiva Câmara; Ronaldo de Carvalho Araújo; José Donato Júnior; Julio Cesar Batista Ferreira; Marco Aurelio Ramirez Vinolo
Advisor: Niels Olsen Saraiva Câmara

Activation of innate immune receptors in immune cells, adipose tissue, and changes in intestinal microbiota were related to inflammatory and metabolic phenotypes during obesity. Here, we hypothesize that MyD88 signaling in certain tissue are critical to those phenotypes observed in obese mice. We observed that MyD88 knockout (KO) mice develop severe metabolic syndrome and decreased IL-1β, TNF-α and IL-6 in adipose tissue despite the predominance of M1 macrophage. In the intestine, we observed decreased inflammation and increased permeability. The microbiota of MyD88 KO mice induced insulin resistance in WT mice. Depletion of MyD88 in adipose tissue did not alter the metabolic profile. However, depletion of MyD88 in macrophages protected mice from metabolic syndrome. In adipose tissue of MyD88 KO obese mice, we observed an increased expression of Dectin-1 and IFN-β. Thus, MyD88 plays an important role in the development of obesity modulating gut microbiota and the inflammatory profile. (AU)

FAPESP's process: 11/15682-4 - Sepsis and obesity: study of the relationship between obesity and immune regulation in an experimental model of sepsis
Grantee:Angela Castoldi
Support type: Scholarships in Brazil - Doctorate