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dc.contributor.authorDuvigneau, Stefanie
dc.contributor.authorSharma-Chawla, Niharika
dc.contributor.authorBoianelli, Alessandro
dc.contributor.authorStegemann-Koniszewski, Sabine
dc.contributor.authorNguyen, Van Kinh
dc.contributor.authorBruder, Dunja
dc.contributor.authorHernandez-Vargas, Esteban Abelardo
dc.date.accessioned2016-12-07T15:07:00Z
dc.date.available2016-12-07T15:07:00Z
dc.date.issued2016-11-22
dc.identifier.citationHierarchical effects of pro-inflammatory cytokines on the post-influenza susceptibility to pneumococcal coinfection. 2016, 6:37045 Sci Repen
dc.identifier.issn2045-2322
dc.identifier.pmid27872472
dc.identifier.doi10.1038/srep37045
dc.identifier.urihttp://hdl.handle.net/10033/620643
dc.description.abstractIn the course of influenza A virus (IAV) infections, a secondary bacterial infection frequently leads to serious respiratory conditions provoking high hospitalization and death tolls. Although abundant pro-inflammatory responses have been reported as key contributing factors for these severe dual infections, the relative contributions of cytokines remain largely unclear. In the current study, mathematical modelling based on murine experimental data dissects IFN-γ as a cytokine candidate responsible for impaired bacterial clearance, thereby promoting bacterial growth and systemic dissemination during acute IAV infection. We also found a time-dependent detrimental role of IL-6 in curtailing bacterial outgrowth which was not as distinct as for IFN-γ. Our numerical simulations suggested a detrimental effect of IFN-γ alone and in synergism with IL-6 but no conclusive pathogenic effect of IL-6 and TNF-α alone. This work provides a rationale to understand the potential impact of how to manipulate temporal immune components, facilitating the formulation of hypotheses about potential therapeutic strategies to treat coinfections.
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleHierarchical effects of pro-inflammatory cytokines on the post-influenza susceptibility to pneumococcal coinfection.en
dc.typeArticleen
dc.contributor.departmentBRICS, Braunschweiger Zentrum für Systembiologie, Rebenring 56, 38106 Braunschweig. Germany.en
dc.identifier.journalScientific reportsen
refterms.dateFOA2018-06-12T22:18:08Z
html.description.abstractIn the course of influenza A virus (IAV) infections, a secondary bacterial infection frequently leads to serious respiratory conditions provoking high hospitalization and death tolls. Although abundant pro-inflammatory responses have been reported as key contributing factors for these severe dual infections, the relative contributions of cytokines remain largely unclear. In the current study, mathematical modelling based on murine experimental data dissects IFN-γ as a cytokine candidate responsible for impaired bacterial clearance, thereby promoting bacterial growth and systemic dissemination during acute IAV infection. We also found a time-dependent detrimental role of IL-6 in curtailing bacterial outgrowth which was not as distinct as for IFN-γ. Our numerical simulations suggested a detrimental effect of IFN-γ alone and in synergism with IL-6 but no conclusive pathogenic effect of IL-6 and TNF-α alone. This work provides a rationale to understand the potential impact of how to manipulate temporal immune components, facilitating the formulation of hypotheses about potential therapeutic strategies to treat coinfections.


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