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Registro Completo

Escolher formato: Padrão Ficha Formato Reduzido Nomes MARC Campos MARC
No. Registro   002479218
Entrada Principal   LinkGarcia, Cristiana C. (*) NAC
Título   LinkComplement C5 activation during influenza A infection in mice contributes to neutrophil recruitment and lung injury.
Imprenta   San Francisco, 2013.
Descrição   p. E64443-1 - E64443-11.
Idioma   Inglês
Nota   Tipo de cobaia utilizada no trabalho de pesquisa : camundongos
Assunto   LinkINFLUENZA
Autor Secundário   LinkWeston-Davies, Wynne (*) INT Varleigh Ltd, London, United Kingdom
  LinkRusso, Remo C. (*) NAC Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil
  LinkTavares, Luciana P. (*) NAC Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil
  LinkRachid, Milene A. (*) NAC Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil
  LinkAlves Filho, José Carlos Farias
  LinkMachado, Alexandre V. (*) NAC Centro de Pesquisas René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, MG
  LinkRyffel, Bernhard (*) INT University Orleans, France and IIDMM, University of Cape Town, Cape Town, South Africa
  LinkNunn, Miles A. (*) INT Centre for Ecology and Hydrology, Wallingford, United Kingdom
  LinkTeixeira, Mauro M. (*) NAC Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil
Fonte   LinkIn: PLoS One, San Francisco, v. 8, n. 5, p. E64443-1 - E64443-11, 2013, ISSN: 1932-6203
Localiz.Eletrônica   e-mail do autor -- mailto://mmtex@icb.ufmg.br
Localiz.Eletrônica    "Clicar" sobre o botão para acesso ao texto completo 
   "Clicar" sobre o botão para acesso ao Currículo Lattes de José Carlos Farias Alves Filho 
   Versão publicada - público 
Resumo/Outros   Influenza virus A (IAV) causes annual epidemics and intermittent pandemics that affect millions of people worldwide. Potent inflammatory responses are commonly associated with severe cases of IAV infection. The complement system, an important mechanism of innate and humoral immune responses to infections, is activated during primary IAV infection and mediates, in association with natural IgM, viral neutralization by virion aggregation and coating of viral hemmagglutinin. Increased levels of the anaphylatoxin C5a were found in patients fatally infected with the most recent H1N1 pandemic virus. In this study, our aim was to evaluate whether targeting C5 activation alters inflammatory lung injury and viral load in a murine model of IAV infection. To address this question C57Bl/6j mice were infected intranasally with ’10 POT. 4’ PFU of the mouse adapted Influenza A virus A/WSN/33 (H1N1) or inoculated with PBS (Mock). We demonstrated that C5a is increased in bronchoalveolar lavage fluid (BALF) upon experimental IAV infection. To evaluate the role of C5, we used OmCI, a potent arthropod-derived inhibitor of C5 activation that binds to C5 and prevents release of C5a by complement. OmCI was given daily by intraperitoneal injection from the day of IAV infection until day 5. Treatment with OmCI only partially reduced C5a levels in BALF. However, there was significant inhibition of neutrophil and macrophage infiltration in the airways, Neutrophil Extracellular Traps (NETs) formation, death of leukocytes, lung epithelial injury and overall lung damage induced by the infection. There was no effect on viral load. Taken together, these data suggest that targeting C5 activation with OmCI during IAV infection could be a promising approach to reduce excessive inflammatory reactions associated with the severe forms of IAV infections
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Escolher formato: Padrão Ficha Formato Reduzido Nomes MARC Campos MARC

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