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Doctoral Thesis
DOI
10.11606/T.42.2010.tde-05102010-121444
Document
Author
Full name
Juciane Maria de Andrade Castro
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2010
Supervisor
Committee
Russo, Momtchilo (President)
Franco, Marcelo de
Martins, Milton de Arruda
Mauro, Eliana Faquim de Lima
Pinto, Frederico Azevedo da Costa
Title in Portuguese
Asma experimental em linhagens de camundongos selecionados para mínima (AIRmin) ou máxima (AIRmax) resposta inflamatória aguda.
Keywords in Portuguese
Alergia
Asma
Camundongos AIRmin e AIRmax
Hiperatividade
Hipersensibilidade
Inflamação
Abstract in Portuguese
Asma é uma doença inflamatória pulmonar crônica usualmente associada com imunidade do tipo 2, eosinofilia pulmonar, hiperreatividade brônquica (AHR), hiper-produção de muco e altos níveis de IgE. Indíviduos asmáticos podem responder aos alérgenos por duas distintas fases: uma fase imediata (EPR) e uma fase tardia (LPR), ambas não reproduzidas na maioria dos modelos murinos de asma. No presente trabalho utilizamos camundongos AIRmax e AIRmin. Verificamos que camundongos AIRmin respondem com uma AHR intrínseca a metacolina. Esta resposta intensa correlacionou-se com uma menor expressão de receptores muscarínicos do tipo 2. Camundongos AIRmax sensibilizados e desafiados com OVA, ao contrário dos AIRmin, desenvolveram LPR e AHR a MCh. Os AIRmax apresentam um denso infiltrado inflamatório com predominância de eosinófilos, uma elevada produção de muco, citocinas (IL-5 e IL-13) e anticorpos anafiláticos IgE e IgG1. De forma surpreendente animais AIRmax desenvolvem quadro alérgico pulmonar crônico que cursa com AHR a MCh e uma inflamação pulmonar com infiltrado de eosinófilos com deposição de colágeno no tecido pulmonar além de uma produção elevada de anticorpos anafiláticos. Em conclusão desenvolvemos um novo modelo murino de asma.
Title in English
Experimental asthma in mice selected for minimum (AIRmin) or maximum (AIRmax) acute inflammatory response.
Keywords in English
Allergy
Asthma
Hyperactivity
Hypersensitivity
Inflammation
Mice AIRmax e AIRmin
Abstract in English
Asthma is a chronic inflammatory lung disease usually associated to Type 2 T helper cells, lung eosinophilia, airway hyper-reactivity (AHR), mucus hyper-secretion and increased titers of IgE. Asthmatic individuals may react to allergens by two distinct phases: an immediate phase (EPR) and a late phase (LPR) both phases were not reproduced in classical murine models of asthma. In the present study we use AIRmax AIRmin mice. We found that AIRmin mice exposed to methacholine presented intense intrinsic AHR. This intense reaction was related to a lower expression of muscarinic type 2 receptors. AIRmax mice sensitized and challenged with OVA, unlike AIRmin developed LPR and AHR to MCh. The AIRmax also developed a dense inflammatory infiltrate containing predominantly eosinophils, hyper-secretion of mucus, cytokines (IL-5 and IL-13) and anaphylactic antibodies (IgE and IgG1). Surprisingly AIRmax mice develop chronic pulmonary allergic framework that leads to AHR to MCh and lung inflammation with eosinophilic infiltration with collagen deposition in lung tissue and a high production of anaphylactic antibodies. In conclusion, we developed a new murine model of asthma.
 
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Publishing Date
2010-10-26
 
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