tetano
Editor, Senior Moderator
Published ahead of print 26 November 2014, doi: 10.1128/JVI.02455-14
Lethal co-infection of influenza virus and Streptococcus pneumoniae lowers antibody response to influenza virus in lung, and reduces germinal center B cells, T follicular helper cells and plasma cells in mediastinal lymph node
Yuet Wu1,
Wenwei Tu1*,
Kwok-Tai Lam1,
Kin-**** Chow2,
Pak-Leung Ho2,
Yi Guan3,
Joseph S. Malik Peiris3 and
Yu-Lung Lau1*
1Department of Paediatrics & Adolescent Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
2Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong, Kong, Hong Kong SAR, China.
3Centre of Influenza Research, School of Public Health, The University of Hong Kong, Hong Kong SAR, China.
ABSTRACT
Secondary Streptococcus pneumoniae infection after influenza is a significant clinical complication resulting in morbidity and sometimes mortality. Prior influenza virus infection has been demonstrated to impair the macrophage and neutrophil response to the subsequent pneumococcal infection. In contrast, how the secondary pneumococcal infection after influenza can affect the adaptive immune response to the initial influenza virus infection is less well understood. Therefore, this study focuses on how secondary pneumococcal infection after influenza may impact on the humoral immune response to the initial influenza virus infection in a lethal co-infection mouse model. When compared to mice infected with influenza virus alone, mice co-infected with influenza virus followed by pneumococcus had significant body weight loss and 100% mortality. In the lung, lethal co-infection significantly increased virus titer, bacterial cell counts and decreased the level of virus specific IgG, IgM and IgA, as well as the number of B cells, CD4 T cells and plasma cells. In spleen, lethal co-infection significantly reduced the size and weight of spleen, as well as the B cells along the follicular developmental lineage. In mediastinal lymph nodes, lethal co-infection significantly decreased germinal center B cells, T follicular helper cells and plasma cells. Adoptive transfer of influenza virus-specific immune serum to co-infected mice improved survival, suggesting the protective functions of anti-influenza virus antibodies. In conclusion, co-infection reduced the B cell response to influenza virus. This study helps us to understand the modulation of B cell response to influenza virus during the lethal co-infection.
Importance: Secondary pneumococcal infection after influenza is an important clinical issue that often results in excess mortality. Since antibodies are key mediator of protection, this study aims to examine the antibody response to influenza virus, and demonstrated that lethal co-infection reduced the B cell response to influenza virus. This study helps to highlight the complexity of the modulation of B cell response in the context of co-infection.
http://jvi.asm.org/content/early/2014/11/20/JVI.02455-14.abstract
Lethal co-infection of influenza virus and Streptococcus pneumoniae lowers antibody response to influenza virus in lung, and reduces germinal center B cells, T follicular helper cells and plasma cells in mediastinal lymph node
Yuet Wu1,
Wenwei Tu1*,
Kwok-Tai Lam1,
Kin-**** Chow2,
Pak-Leung Ho2,
Yi Guan3,
Joseph S. Malik Peiris3 and
Yu-Lung Lau1*
1Department of Paediatrics & Adolescent Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
2Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong, Kong, Hong Kong SAR, China.
3Centre of Influenza Research, School of Public Health, The University of Hong Kong, Hong Kong SAR, China.
ABSTRACT
Secondary Streptococcus pneumoniae infection after influenza is a significant clinical complication resulting in morbidity and sometimes mortality. Prior influenza virus infection has been demonstrated to impair the macrophage and neutrophil response to the subsequent pneumococcal infection. In contrast, how the secondary pneumococcal infection after influenza can affect the adaptive immune response to the initial influenza virus infection is less well understood. Therefore, this study focuses on how secondary pneumococcal infection after influenza may impact on the humoral immune response to the initial influenza virus infection in a lethal co-infection mouse model. When compared to mice infected with influenza virus alone, mice co-infected with influenza virus followed by pneumococcus had significant body weight loss and 100% mortality. In the lung, lethal co-infection significantly increased virus titer, bacterial cell counts and decreased the level of virus specific IgG, IgM and IgA, as well as the number of B cells, CD4 T cells and plasma cells. In spleen, lethal co-infection significantly reduced the size and weight of spleen, as well as the B cells along the follicular developmental lineage. In mediastinal lymph nodes, lethal co-infection significantly decreased germinal center B cells, T follicular helper cells and plasma cells. Adoptive transfer of influenza virus-specific immune serum to co-infected mice improved survival, suggesting the protective functions of anti-influenza virus antibodies. In conclusion, co-infection reduced the B cell response to influenza virus. This study helps us to understand the modulation of B cell response to influenza virus during the lethal co-infection.
Importance: Secondary pneumococcal infection after influenza is an important clinical issue that often results in excess mortality. Since antibodies are key mediator of protection, this study aims to examine the antibody response to influenza virus, and demonstrated that lethal co-infection reduced the B cell response to influenza virus. This study helps to highlight the complexity of the modulation of B cell response in the context of co-infection.
http://jvi.asm.org/content/early/2014/11/20/JVI.02455-14.abstract