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@ARTICLE{Oliveira:284089,
      author       = {Oliveira, Lorena V. N. and Costa, Marliete C. and
                      Magalhães, Thaís F. F. and Bastos, Rafael W. and Campi
                      Santos, Patricia and Carneiro, Hellem C. S. and Ribeiro,
                      Noelly Q. and Ferreira, Gabriella F. and Secchim Ribeiro,
                      Lucas and Gonçalves, Ana P. F. and Fagundes, Caio T. and
                      Pascoal-Xavier, Marcelo A. and Djordjevic, Julianne T. and
                      Sorrell, Tania C. and Souza, Daniele G. and Machado,
                      Alexandre M. V. and Santos, Daniel A.},
      title        = {{I}nfluenza {A} {V}irus as a {P}redisposing {F}actor for
                      {C}ryptococcosis},
      journal      = {Frontiers in Cellular and Infection Microbiology},
      volume       = {7},
      issn         = {2235-2988},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DZNE-2026-00097},
      pages        = {419},
      year         = {2017},
      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.},
      keywords     = {Acetylglucosaminidase: metabolism / Animals / Behavior,
                      Animal / Brain: microbiology / Brain: pathology / Causality
                      / Cell Proliferation / Chemokines: metabolism / Coinfection:
                      immunology / Coinfection: microbiology / Coinfection:
                      mortality / Coinfection: virology / Cryptococcosis:
                      complications / Cryptococcosis: immunology / Cryptococcus
                      gattii: immunology / Cryptococcus gattii: pathogenicity /
                      Cryptococcus neoformans: immunology / Cytokines: metabolism
                      / Disease Models, Animal / Disease Susceptibility / Dogs /
                      Female / Humans / Influenza A Virus, H1N1 Subtype:
                      immunology / Influenza A Virus, H1N1 Subtype: pathogenicity
                      / Interferon-gamma: metabolism / Lung: enzymology / Lung:
                      pathology / Lung: virology / Macrophages: metabolism /
                      Macrophages: virology / Madin Darby Canine Kidney Cells /
                      Mice / Mice, Inbred C57BL / Neutrophils / Nitric Oxide:
                      metabolism / Orthomyxoviridae Infections: complications /
                      Orthomyxoviridae Infections: immunology / Peroxidase:
                      metabolism / Peroxynitrous Acid: metabolism / Phagocytosis /
                      Reactive Oxygen Species: metabolism / Survival Rate /
                      Cryptococcosis (Other) / Cryptococcus gattii (Other) /
                      co-infection (Other) / influenza A H1N1 (Other) / risk
                      factor (Other) / Chemokines (NLM Chemicals) / Cytokines (NLM
                      Chemicals) / IFNG protein, mouse (NLM Chemicals) / Reactive
                      Oxygen Species (NLM Chemicals) / Peroxynitrous Acid (NLM
                      Chemicals) / Nitric Oxide (NLM Chemicals) / Interferon-gamma
                      (NLM Chemicals) / Peroxidase (NLM Chemicals) /
                      Acetylglucosaminidase (NLM Chemicals)},
      ddc          = {610},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.3389/fcimb.2017.00419},
      url          = {https://pub.dzne.de/record/284089},
}