Influenza A Virus as a Predisposing Factor for Cryptococcosis.

Autor: Oliveira LVN; Laboratório de Micologia, Departamento de Microbiologia, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Belo Horizonte, Brazil., Costa MC; Laboratório de Micologia, Departamento de Microbiologia, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Belo Horizonte, Brazil., Magalhães TFF; Laboratório de Micologia, Departamento de Microbiologia, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Belo Horizonte, Brazil., Bastos RW; Laboratório de Micologia, Departamento de Microbiologia, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Belo Horizonte, Brazil., Santos PC; Laboratório de Interação Micro-organismo Hospedeiro, Departamento de Microbiologia, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Belo Horizonte, Brazil., Carneiro HCS; Laboratório de Micologia, Departamento de Microbiologia, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Belo Horizonte, Brazil., Ribeiro NQ; Laboratório de Micologia, Departamento de Microbiologia, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Belo Horizonte, Brazil., Ferreira GF; Departamento de Farmácia, Universidade Federal de Juiz de Fora-Campus Governador Valadares, Centro, Governador Valadares, Brazil., Ribeiro LS; Laboratório de Interação Micro-organismo Hospedeiro, Departamento de Microbiologia, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Belo Horizonte, Brazil., Gonçalves APF; Centro de Pesquisas René Rachou (CPqRR)/Fundação Oswaldo Cruz (Fiocruz Minas), Belo Horizonte, Brazil., Fagundes CT; Laboratório de Interação Micro-organismo Hospedeiro, Departamento de Microbiologia, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Belo Horizonte, Brazil.; Centro de Pesquisa e Desenvolvimento de Fármacos, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Belo Horizonte, Brazil., Pascoal-Xavier MA; Centro de Pesquisas René Rachou (CPqRR)/Fundação Oswaldo Cruz (Fiocruz Minas), Belo Horizonte, Brazil., Djordjevic JT; Marie Bashir Institute for Infectious Diseases and Biosecurity, University of Sydney and Westmead Institute for Medical Research, Westmead, NSW, Australia., Sorrell TC; Marie Bashir Institute for Infectious Diseases and Biosecurity, University of Sydney and Westmead Institute for Medical Research, Westmead, NSW, Australia., Souza DG; Laboratório de Interação Micro-organismo Hospedeiro, Departamento de Microbiologia, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Belo Horizonte, Brazil., Machado AMV; Centro de Pesquisas René Rachou (CPqRR)/Fundação Oswaldo Cruz (Fiocruz Minas), Belo Horizonte, Brazil., Santos DA; Laboratório de Micologia, Departamento de Microbiologia, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Jazyk: angličtina
Zdroj: Frontiers in cellular and infection microbiology [Front Cell Infect Microbiol] 2017 Sep 26; Vol. 7, pp. 419. Date of Electronic Publication: 2017 Sep 26 (Print Publication: 2017).
DOI: 10.3389/fcimb.2017.00419
Abstrakt: Influenza A virus (IAV) infects millions of people annually and predisposes to secondary bacterial infections. Inhalation of fungi within the Cryptococcus complex causes pulmonary disease with secondary meningo-encephalitis. Underlying pulmonary disease is a strong risk factor for development of C. gattii cryptococcosis though the effect of concurrent infection with IAV has not been studied. We developed an in vivo model of Influenza A H1N1 and C. gattii co-infection. Co-infection resulted in a major increase in morbidity and mortality, with severe lung damage and a high brain fungal burden when mice were infected in the acute phase of influenza multiplication. Furthermore, IAV alters the host response to C. gattii , leading to recruitment of significantly more neutrophils and macrophages into the lungs. Moreover, IAV induced the production of type 1 interferons (IFN-α4/β) and the levels of IFN-γ were significantly reduced, which can be associated with impairment of the immune response to Cryptococcus during co-infection. Phagocytosis, killing of cryptococci and production of reactive oxygen species (ROS) by IAV-infected macrophages were reduced, independent of previous IFN-γ stimulation, leading to increased proliferation of the fungus within macrophages. In conclusion, IAV infection is a predisposing factor for severe disease and adverse outcomes in mice co-infected with C. gattii .
Databáze: MEDLINE