Bordetella pertussis modulates human macrophage defense gene expression

<i>Bordetella pertussis</i>, the etiological agent of whooping cough, still causes outbreaks. We recently found evidence that <i>B. pertussis</i> can survive and even replicate inside human macrophages, indicating that this host cell might serve as a niche for persistence. In...

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Detalhes bibliográficos
Autores: Valdez, Hugo Alberto, Oviedo, Juan Marcos, Gorgojo, Juan Pablo, Lamberti, Yanina Andrea, Rodríguez, María Eugenia
Tipo de documento: artigo
Estado:Versão publicada
Data de publicação:2016
País:Argentina
Recursos:Universidad Nacional de La Plata
Repositório:SEDICI (UNLP)
Idioma:inglês
OAI Identifier:oai:sedici.unlp.edu.ar:10915/85803
Acesso em linha:http://sedici.unlp.edu.ar/handle/10915/85803
Access Level:Acceso aberto
Palavra-chave:Ciencias Exactas
Adenylate cyclase
Bordetella pertussis
Host cell defense response
Intracellular survival
Pertussis toxin
Descrição
Resumo:<i>Bordetella pertussis</i>, the etiological agent of whooping cough, still causes outbreaks. We recently found evidence that <i>B. pertussis</i> can survive and even replicate inside human macrophages, indicating that this host cell might serve as a niche for persistence. In this work, we examined the interaction of <i>B. pertussis</i> with a human monocyte cell line (THP-1) that differentiates into macrophages in culture in order to investigate the host cell response to the infection and the mechanisms that promote that intracellular survival. To that end, we investigated the expression profile of a selected number of genes involved in cellular bactericidal activity and the inflammatory response during the early and late phases of infection. The bactericidal and inflammatory response of infected macrophages was progressively downregulated, while the number of THP-1 cells heavily loaded with live bacteria increased over time postinfection. Two of the main toxins of <i>B. pertussis</i>, pertussis toxin (Ptx) and adenylate cyclase (CyaA), were found to be involved in manipulating the host cell response. Therefore, failure to express either toxin proved detrimental to the development of intracellular infections by those bacteria. Taken together, these results support the relevance of host defense gene manipulation to the outcome of the interaction between <i>B. pertussis</i> and macrophages.