tetano
Editor, Senior Moderator
Vaccines (Basel). 2019 Sep 12;7(3). pii: E113. doi: 10.3390/vaccines7030113.
[h=1]TIV Vaccination Modulates Host Responses to Influenza Virus Infection that Correlate with Protection against Bacterial Superinfection.[/h] Choi A[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Christopoulou I[SUP]4[/SUP], Saelens X[SUP]5[/SUP], Garc?a-Sastre A[SUP]6,[/SUP][SUP]7,[/SUP][SUP]8,[/SUP][SUP]9[/SUP], Schotsaert M[SUP]10,[/SUP][SUP]11[/SUP].
[h=3]Author information[/h] 1 Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Angela.Choi@Icahn.mssm.edu. 2 Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Angela.Choi@Icahn.mssm.edu. 3 Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Angela.Choi@Icahn.mssm.edu. 4 VIB-UGent Center for Medical Biotechnology, Department of Biomedical Molecular Biology, Ghent University 9000-9052 Ghent, Belgium. ioannachristopoulou@googlemail.com. 5 VIB-UGent Center for Medical Biotechnology, Department of Biomedical Molecular Biology, Ghent University 9000-9052 Ghent, Belgium. Xavier.Saelens@ugent.vib.be. 6 Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Adolfo.Garcia-Sastre@mssm.edu. 7 Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Adolfo.Garcia-Sastre@mssm.edu. 8 Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Adolfo.Garcia-Sastre@mssm.edu. 9 The Tish Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Adolfo.Garcia-Sastre@mssm.edu. 10 Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. michael.schotsaert@mssm.edu. 11 Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. michael.schotsaert@mssm.edu.
[h=3]Abstract[/h] [h=4]BACKGROUND:[/h] Influenza virus infection predisposes to secondary bacterial pneumonia. Currently licensed influenza vaccines aim at the induction of neutralizing antibodies and are less effective if the induction of neutralizing antibodies is low and/or the influenza virus changes its antigenic surface. We investigated the effect of suboptimal vaccination on the outcome of post-influenza bacterial superinfection.
[h=4]METHODS:[/h] We established a mouse vaccination model that allows control of disease severity after influenza virus infection despite inefficient induction of virus-neutralizing antibody titers by vaccination. We investigated the effect of vaccination on virus-induced host immune responses and on the outcome of superinfection with Staphylococcus aureus.
[h=4]RESULTS:[/h] Vaccination with trivalent inactivated virus vaccine (TIV) reduced morbidity after influenza A virus infection but did not prevent virus replication completely. Despite the poor induction of influenza-specific antibodies, TIV protected from mortality after bacterial superinfection. Vaccination limited loss of alveolar macrophages and reduced levels of infiltrating pulmonary monocytes after influenza virus infection. Interestingly, TIV vaccination resulted in enhanced levels of eosinophils after influenza virus infection and recruitment of neutrophils in both lungs and mediastinal lymph nodes after bacterial superinfection.
[h=4]CONCLUSION:[/h] These observations highlight the importance of disease modulation by influenza vaccination, even when suboptimal, and suggest that influenza vaccination is still beneficial to protect during bacterial superinfection in the absence of complete virus neutralization.
[h=4]KEYWORDS:[/h] Staphylococcus aureus; TIV; bacterial superinfection; eosinophil; influenza; macrophage; neutrophil
PMID: 31547409 DOI: 10.3390/vaccines7030113
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[h=1]TIV Vaccination Modulates Host Responses to Influenza Virus Infection that Correlate with Protection against Bacterial Superinfection.[/h] Choi A[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Christopoulou I[SUP]4[/SUP], Saelens X[SUP]5[/SUP], Garc?a-Sastre A[SUP]6,[/SUP][SUP]7,[/SUP][SUP]8,[/SUP][SUP]9[/SUP], Schotsaert M[SUP]10,[/SUP][SUP]11[/SUP].
[h=3]Author information[/h] 1 Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Angela.Choi@Icahn.mssm.edu. 2 Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Angela.Choi@Icahn.mssm.edu. 3 Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Angela.Choi@Icahn.mssm.edu. 4 VIB-UGent Center for Medical Biotechnology, Department of Biomedical Molecular Biology, Ghent University 9000-9052 Ghent, Belgium. ioannachristopoulou@googlemail.com. 5 VIB-UGent Center for Medical Biotechnology, Department of Biomedical Molecular Biology, Ghent University 9000-9052 Ghent, Belgium. Xavier.Saelens@ugent.vib.be. 6 Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Adolfo.Garcia-Sastre@mssm.edu. 7 Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Adolfo.Garcia-Sastre@mssm.edu. 8 Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Adolfo.Garcia-Sastre@mssm.edu. 9 The Tish Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Adolfo.Garcia-Sastre@mssm.edu. 10 Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. michael.schotsaert@mssm.edu. 11 Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. michael.schotsaert@mssm.edu.
[h=3]Abstract[/h] [h=4]BACKGROUND:[/h] Influenza virus infection predisposes to secondary bacterial pneumonia. Currently licensed influenza vaccines aim at the induction of neutralizing antibodies and are less effective if the induction of neutralizing antibodies is low and/or the influenza virus changes its antigenic surface. We investigated the effect of suboptimal vaccination on the outcome of post-influenza bacterial superinfection.
[h=4]METHODS:[/h] We established a mouse vaccination model that allows control of disease severity after influenza virus infection despite inefficient induction of virus-neutralizing antibody titers by vaccination. We investigated the effect of vaccination on virus-induced host immune responses and on the outcome of superinfection with Staphylococcus aureus.
[h=4]RESULTS:[/h] Vaccination with trivalent inactivated virus vaccine (TIV) reduced morbidity after influenza A virus infection but did not prevent virus replication completely. Despite the poor induction of influenza-specific antibodies, TIV protected from mortality after bacterial superinfection. Vaccination limited loss of alveolar macrophages and reduced levels of infiltrating pulmonary monocytes after influenza virus infection. Interestingly, TIV vaccination resulted in enhanced levels of eosinophils after influenza virus infection and recruitment of neutrophils in both lungs and mediastinal lymph nodes after bacterial superinfection.
[h=4]CONCLUSION:[/h] These observations highlight the importance of disease modulation by influenza vaccination, even when suboptimal, and suggest that influenza vaccination is still beneficial to protect during bacterial superinfection in the absence of complete virus neutralization.
[h=4]KEYWORDS:[/h] Staphylococcus aureus; TIV; bacterial superinfection; eosinophil; influenza; macrophage; neutrophil
PMID: 31547409 DOI: 10.3390/vaccines7030113
Free full text