GEA SUSANA ELBA
Congresos y reuniones científicas
Título:
The Impact of Trypanosoma Cruzi Infection on the Evolution of Cardiovascular and Liver Disease Induced by Fat Diet: The Significance of Toll Like Receptor-4
Reunión:
Simposio; International Symposium on Immunonutrition 2017, Madrid, 17th-19th July, 2017; 2017
Institución organizadora:
Sociedad Internacional de Inmunonutricion
Resumen:
The impact of Trypanosoma cruzi infection on the evolution of cardiovascular and liver disease induced by fat diet: the significance of Toll Like Receptor-4Abstract: aim, method, key findings, conclusionObesity is considered an epidemic inflammatory disease with great impact on human health. The metabolic syndrome (MS) is associated with cardiovascular and liver disease. Previously we developed a MS model in C57BL/6 WT fed with fat diet after 4 months1. Objective: To elucidate the effect of T. cruzi infection in the pathogenesis of MS and investigate the role of TLR4 innate receptor in this process. Thus, male C57BL/6 mice WT and TLR4-/ - mice were divided into 4 groups B, basal with standard feed (3% fat), D, 13% fat diet, I (100 T. cruzi parasites-Tulahuén) and I+D, Infected+Diet. Results: There was an increase in body weight in D-WT vs B (p<0.001). Besides, this group showed adipocyte hypertrophy in aortic adventitia and lipid micro/macrovesículas and inflammatory foci compatible with steatohepatitis, not observable in TLR4-/-. Notably, the groups I+D (WT and KO) didn`t show ectopic fat but showed an increased number of liver leukocytes. A significant increase of CD36 expression was detected in the liver and aorta only in D-WT. F4/80+CD68+CD206- cells were observed in liver of animals D and I+D vs B only in WT(p<0.05). CD8+ T cells were increased in D-WT group. The % of CD8+IFNy+ cells was increased in group D-WT vs B. There was also an increase in the % of CD4+ and CD8+ in I+D-WT. Conclusion:These results clearly demonstrate the involvement of TLR4 receptor in the model of MS, and parasite infection improves steatohepatitis and lipid deposition in the aorta but increases the number of inflammatory cells.AcknowledgmentsThe authors would like to thank Alejandra Romero, Pilar Crespo, Paula Abadie and Fabricio Navarro for their skillful technical assistance.Financial SupportAgencia Nacional de Promoción Científica y Tecnológica (ANPCYT-PICT 2013-2104); Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) PIP 20102 and Secretaría de Ciencia y Técnica de la Universidad Nacional de Córdoba (SECYT-UNC) 2014, Córdoba, Argentina.