Autophagy induction favours the generation and maturation of the Coxiella-replicative vacuoles

Autophagy induction favours the generation and maturation of the Coxiella-replicative vacuoles

Autor Gutierrez, M. G. Google Scholar
Vazquez, C. L. Google Scholar
Munafo, D. B. Google Scholar
Zoppino, FCM Google Scholar
Beron, W. Google Scholar
Rabinovitch, M. Autor UNIFESP Google Scholar
Colombo, M. I. Google Scholar
Instituição Univ Nacl Cuyo
Universidade Federal de São Paulo (UNIFESP)
Resumo Pathogens evolved mechanisms to invade host cells and to multiply in the cytosol or in compositionally and functionally customized membrane-bound compartments. Coxiella burnetii, the agent of Q fever in man is a Gram-negative gamma-proteobacterium which multiplies in large, acidified, hydrolase-rich and fusogenic vacuoles with phagolysosomal-like characteristics. We reported previously that C. burnetii phase II replicative compartments are labelled by LC3, a protein specifically localized to autophagic vesicles. We show here that autophagy in Chinese hamster ovary cells, induced by amino acid deprivation prior to infection with Coxiella increased the number of infected cells, the size of the vacuoles, and their bacterial load. Furthermore, overexpression of GFP-LC3 or of GFP-Rab24 - a protein also localized to autophagic vacuoles - likewise accelerated the development of Coxiella-vacuoles at early times after infection. However, overexpression of mutants of those proteins that cannot be targeted to autophagosomes dramatically decreased the number and size of the vacuoles in the first hours of infection, although by 48 h the infection was similar to that of non-transfected controls. Overall, the results suggest that transit through the autophagic pathway increases the infection with Coxiella by providing a niche more favourable to their initial survival and multiplication.
Idioma Inglês
Data 2005-07-01
Publicado em Cellular Microbiology. Hoboken: Wiley-Blackwell, v. 7, n. 7, p. 981-993, 2005.
ISSN 1462-5814 (Sherpa/Romeo, fator de impacto)
Editor Wiley-Blackwell
Extensão 981-993
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000229679900008

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