Hierarchical effects of pro-inflammatory cytokines on the post-influenza susceptibility to pneumococcal coinfection.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
Nguyen, Van Kinh
Hernandez-Vargas, Esteban Abelardo
MetadataShow full item record
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.
CitationHierarchical effects of pro-inflammatory cytokines on the post-influenza susceptibility to pneumococcal coinfection. 2016, 6:37045 Sci Rep
AffiliationBRICS, Braunschweiger Zentrum für Systembiologie, Rebenring 56, 38106 Braunschweig. Germany.
The following license files are associated with this item:
- Creative Commons
Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by-nc-sa/4.0/
- <i>In vivo</i> Neutralization of Pro-inflammatory Cytokines During Secondary <i>Streptococcus pneumoniae</i> Infection Post Influenza A Virus Infection.
- Authors: Sharma-Chawla N, Stegemann-Koniszewski S, Christen H, Boehme JD, Kershaw O, Schreiber J, Guzmán CA, Bruder D, Hernandez-Vargas EA
- Issue date: 2019
- Linezolid decreases susceptibility to secondary bacterial pneumonia postinfluenza infection in mice through its effects on IFN-γ.
- Authors: Breslow-Deckman JM, Mattingly CM, Birket SE, Hoskins SN, Ho TN, Garvy BA, Feola DJ
- Issue date: 2013 Aug 15
- Lethal coinfection of influenza virus and Streptococcus pneumoniae lowers antibody response to influenza virus in lung and reduces numbers of germinal center B cells, T follicular helper cells, and plasma cells in mediastinal lymph Node.
- Authors: Wu Y, Tu W, Lam KT, Chow KH, Ho PL, Guan Y, Peiris JS, Lau YL
- Issue date: 2015 Feb
- TRAIL+ monocytes and monocyte-related cells cause lung damage and thereby increase susceptibility to influenza-Streptococcus pneumoniae coinfection.
- Authors: Ellis GT, Davidson S, Crotta S, Branzk N, Papayannopoulos V, Wack A
- Issue date: 2015 Sep
- Increase of apoptosis in a murine model for severe pneumococcal pneumonia during influenza A virus infection.
- Authors: Kosai K, Seki M, Tanaka A, Morinaga Y, Imamura Y, Izumikawa K, Kakeya H, Yamamoto Y, Yanagihara K, Tomono K, Kohno S
- Issue date: 2011