Journal Article

DZNE-2026-00097

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Influenza A Virus as a Predisposing Factor for Cryptococcosis

Oliveira, L. V. N. ; Costa, M. C. ; Magalhães, T. F. F. ; Bastos, R. W. ; Campi Santos, P.Extern* ; Carneiro, H. C. S. ; Ribeiro, N. Q. ; Ferreira, G. F. ; Secchim Ribeiro, L.Extern* ; Gonçalves, A. P. F. ; Fagundes, C. T. ; Pascoal-Xavier, M. A. ; Djordjevic, J. T. ; Sorrell, T. C. ; Souza, D. G. ; Machado, A. M. V. ; Santos, D. A.

2017
Frontiers Media Lausanne

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Please use a persistent id in citations: doi:10.3389/fcimb.2017.00419

Abstract: 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.

Keyword(s): Acetylglucosaminidase: metabolism (MeSH) ; Animals (MeSH) ; Behavior, Animal (MeSH) ; Brain: microbiology (MeSH) ; Brain: pathology (MeSH) ; Causality (MeSH) ; Cell Proliferation (MeSH) ; Chemokines: metabolism (MeSH) ; Coinfection: immunology (MeSH) ; Coinfection: microbiology (MeSH) ; Coinfection: mortality (MeSH) ; Coinfection: virology (MeSH) ; Cryptococcosis: complications (MeSH) ; Cryptococcosis: immunology (MeSH) ; Cryptococcus gattii: immunology (MeSH) ; Cryptococcus gattii: pathogenicity (MeSH) ; Cryptococcus neoformans: immunology (MeSH) ; Cytokines: metabolism (MeSH) ; Disease Models, Animal (MeSH) ; Disease Susceptibility (MeSH) ; Dogs (MeSH) ; Female (MeSH) ; Humans (MeSH) ; Influenza A Virus, H1N1 Subtype: immunology (MeSH) ; Influenza A Virus, H1N1 Subtype: pathogenicity (MeSH) ; Interferon-gamma: metabolism (MeSH) ; Lung: enzymology (MeSH) ; Lung: pathology (MeSH) ; Lung: virology (MeSH) ; Macrophages: metabolism (MeSH) ; Macrophages: virology (MeSH) ; Madin Darby Canine Kidney Cells (MeSH) ; Mice (MeSH) ; Mice, Inbred C57BL (MeSH) ; Neutrophils (MeSH) ; Nitric Oxide: metabolism (MeSH) ; Orthomyxoviridae Infections: complications (MeSH) ; Orthomyxoviridae Infections: immunology (MeSH) ; Peroxidase: metabolism (MeSH) ; Peroxynitrous Acid: metabolism (MeSH) ; Phagocytosis (MeSH) ; Reactive Oxygen Species: metabolism (MeSH) ; Survival Rate (MeSH) ; Cryptococcosis ; Cryptococcus gattii ; co-infection ; influenza A H1N1 ; risk factor ; Chemokines ; Cytokines ; IFNG protein, mouse ; Reactive Oxygen Species ; Peroxynitrous Acid ; Nitric Oxide ; Interferon-gamma ; Peroxidase ; Acetylglucosaminidase

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Research Program(s):

1. 899 - ohne Topic (POF4-899) (POF4-899)

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