Increased survival and proliferation of the epidemic strain Mycobacterium abscessus subsp massiliense CRM0019 in alveolar epithelial cells

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dc.contributor.author Ribeiro, Giovanni Monteiro [UNIFESP]
dc.contributor.author Matsumoto, Cristianne Kayoko [UNIFESP]
dc.contributor.author Real, Fernando [UNIFESP]
dc.contributor.author Teixeira, Daniela [UNIFESP]
dc.contributor.author Duarte, Rafael Silva
dc.contributor.author Mortara, Renato Arruda [UNIFESP]
dc.contributor.author Leao, Sylvia Cardoso [UNIFESP]
dc.contributor.author Carvalho-Wodarz, Cristiane de Souza [UNIFESP]
dc.date.accessioned 2020-08-04T13:40:12Z
dc.date.available 2020-08-04T13:40:12Z
dc.date.issued 2017
dc.identifier http://dx.doi.org/10.1186/s12866-017-1102-7
dc.identifier.citation Bmc Microbiology. London, v. 17, p. -, 2017.
dc.identifier.issn 1471-2180
dc.identifier.uri https://repositorio.unifesp.br/handle/11600/57360
dc.description.abstract Background: Outbreaks of infections caused by rapidly growing mycobacteria have been reported worldwide generally associated with medical procedures. Mycobacterium abscessus subsp. massiliense CRM0019 was obtained during an epidemic of postsurgical infections and was characterized by increased persistence in vivo. To better understand the successful survival strategies of this microorganism, we evaluated its infectivity and proliferation in macrophages (RAW and BMDM) and alveolar epithelial cells (A549). For that, we assessed the following parameters, for both M. abscessus CRM0019 as well as the reference strain M. abscessus ATCC 19977: internalization, intracellular survival for up 3 days, competence to subvert lysosome fusion and the intracellular survival after cell reinfection. Results: CRM0019 and ATCC 19977 strains showed the same internalization rate (approximately 30% after 6 h infection), in both A549 and RAW cells. However, colony forming units data showed that CRM0019 survived better in A549 cells than the ATCC 19977 strain. Phagosomal characteristics of CRM0019 showed the bacteria inside tight phagosomes in A549 cells, contrasting to the loosely phagosomal membrane in macrophages. This observation holds for the ATCC 19977 strain in both cell types. The competence to subvert lysosome fusion was assessed by acidification and acquisition of lysosomal protein. For M. abscessus strains the phagosomes were acidified in all cell lines en
dc.description.abstract nevertheless, the acquisition of lysosomal protein was reduced by CRM0019 compared to the ATCC 19977 strain, in A549 cells. Conversely, in macrophages, both M. abscessus strains were located in mature phagosomes, however without bacterial death. Once recovered from macrophages M. abscessus could establish a new intracellular infection. Nevertheless, only CRM0019 showed a higher growth rate in A549, increasing nearly 10- fold after 48 and 72 h. Conclusion: M. abscessus CRM0019 creates a protective and replicative niche in alveolar epithelial cells mainly by avoiding phagosome maturation. Once recovered from infected macrophages, CRM0019 remains infective and displays greater intracellular growth in A549 cells compared to the ATCC 19977 strain. This evasion strategy in alveolar epithelial cells may contribute to the long survival of the CRM0019 strain in the host and thus to the inefficacy of in vivo treatment. en
dc.description.sponsorship Sao Paulo Research Foundation (FAPESP)
dc.format.extent -
dc.language.iso eng
dc.publisher Biomed Central Ltd
dc.relation.ispartof Bmc Microbiology
dc.rights Acesso aberto
dc.subject Mycobacterium abscessus en
dc.subject Phagosome en
dc.subject Acidification en
dc.subject A549 en
dc.subject Macrophages en
dc.subject CRM0019 en
dc.title Increased survival and proliferation of the epidemic strain Mycobacterium abscessus subsp massiliense CRM0019 in alveolar epithelial cells en
dc.type Artigo
dc.description.affiliation Univ Fed Sao Paulo, Escola Paulista Med, Dept Microbiol Imunol & Parasitol, Sao Paulo, SP, Brazil
dc.description.affiliation Inst Cochin, Dept Infect Immunite & Inflammat, Lab Entree Muqueuse VIH & Immunite Muqueuse, Paris, France
dc.description.affiliation Inst Microbiol Prof Paulo de Goes, Lab Micobacterias, Cidade Univ, Rio De Janeiro, Brazil
dc.description.affiliation Helmholtz Ctr Infect Res HZI, Helmholtz Inst Pharmaceut Res Saarland HIPS, Dept Drug Delivery, Saarbrucken, Germany
dc.description.affiliationUnifesp Univ Fed Sao Paulo, Escola Paulista Med, Dept Microbiol Imunol & Parasitol, Sao Paulo, SP, Brazil
dc.description.sponsorshipID FAPESP: 2012/04913-8
dc.description.sponsorshipID FAPESP: 2013/16018-6
dc.description.sponsorshipID FAPESP: 2009/14665-9
dc.identifier.file WOS000410951100002.pdf
dc.identifier.doi 10.1186/s12866-017-1102-7
dc.description.source Web of Science
dc.identifier.wos WOS:000410951100002
dc.coverage London
dc.citation.volume 17



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