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Doctoral Thesis
DOI
10.11606/T.42.2013.tde-15032014-111816
Document
Author
Full name
Lorena Bavia
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2013
Supervisor
Committee
Isaac, Lourdes (President)
Camarini, Rosana
Chammas, Roger
Franco, Marcelo de
Pinge Filho, Phileno
Title in Portuguese
Contribuição do componente C5 do sistema complemento em modelo experimental murino de doença hepática alcoólica.
Keywords in Portuguese
Camundongos
Citocinas
Imunidade ativa
Inflamação
Nucleotídeos
Sistema complemento
Abstract in Portuguese
O sistema complemento participa da patogenia da Doença Hepática Alcoólica (DHA), onde C3 contribui para o acúmulo de triglicerídeos (tg) e C5 para injúria e inflamação hepática. Investigamos o papel de C5 em modelo de DHA aplicando as linhagens B6 e A/J, e geramos a linhagem congênica B6.A-Hc0 (B6 C5def). B6 e A/J foram tratados com dieta contendo ou não etanol, ou maltodextrina, por 6, 8 e 10 semanas. Em ambas as linhagens a dieta com etanol induziu hepatomegalia, acúmulo de tg e redução de IL6 e IL12 hepáticos ao longo das semanas. Os A/J tratados com etanol exibiram aumento de leucócitos circulantes, IL10 e NO hepáticos e menor acúmulo de tg hepáticos em relação aos B6. Os B6 tratados com etanol exibiram redução de IL1b, IL10 e NO hepáticos. Tratando a linhagem congênica por 10 semanas com a dieta com etanol observamos aumento de IL17 e IL10 e redução de IL1b e TGFb hepáticos nos B6.A-Hc0 em relação aos B6. Independentemente da dieta, houve aumento sérico de AST, FA, albumina, colesterol, tg e redução hepática de IL6, IL12 e IFNg nos B6.A-Hc0. Portanto, C5 promoveu um ambiente hepático pró-inflamatório e pareceu influenciar os valores séricos das enzimas de função e síntese hepática, citocinas e do perfil lipídico no modelo de DHA.
Title in English
Contribution of murine complement component C5 in experimental alcoholic fatty liver disease.
Keywords in English
Active immunity
Complement system
Cytokines
Inflammation
Mice
Nucleotides
Abstract in English
The complement system may be involved in the pathogenesis of Alcoholic Fatty Liver Disease (ALD). Murine models of ALD showed that C3 contributes to the accumulation of triglycerides (tg) in liver and the C5 seems to be involved with hepatic inflammation. We here investigated the contribution of C5 in ALD using C57Bl/6 (B6) and A/J (C5 deficient), and B6 C5 deficient congenic mice (B6.A-Hc0). B6 and A/J were treated with modified diet containing ethanol or maltodextrin for 6-10 weeks. In both strains, the ethanol diet induced hepatomegaly, increased liver tg and decreased IL6 and IL12 levels. However, total blood leukocytes counting, IL10 and NO liver production increased only in A/J. In addition, only in B6 the IL1b levels increased while IL10 and NO decreased in liver. A/J mice suffered more inflammatory damage and accumulated less liver tg than B6. In B6.A-Hc0 IL17 and IL10 increased while of IL1b and TGFb decreased when compared to B6. Independently of the diet, levels of AST, FA, albumin, cholesterol, tg increased in B6.A-Hc0 serum and IL6, IL12 and IFNg reduced in liver. In conclusion, C5 promoted a pro-inflammatory environment in the liver and influenced the serum levels of hepatic enzymes, cytokines and lipid profile.
 
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Publishing Date
2014-03-29
 
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