tetano
Editor, Senior Moderator
J Immunol. 2014 Oct 13. pii: 1400529. [Epub ahead of print]
Coinfection with Streptococcus pneumoniae Negatively Modulates the Size and Composition of the Ongoing Influenza-Specific CD8+ T Cell Response.
Blevins LK1, Wren JT1, Holbrook BC1, Hayward SL1, Swords WE1, Parks GD1, Alexander-Miller MA2.
Author information
Abstract
Infection with influenza A virus can lead to increased susceptibility to subsequent bacterial infection, often with Streptococcus pneumoniae. Given the substantial modification of the lung environment that occurs following pathogen infection, there is significant potential for modulation of immune responses. In this study, we show that infection of mice with influenza virus, followed by the noninvasive EF3030 strain of Streptococcus pneumoniae, leads to a significant decrease in the virus-specific CD8+ T cell response in the lung. Adoptive-transfer studies suggest that this reduction contributes to disease in coinfected animals. The reduced number of lung effector cells in coinfected animals was associated with increased death, as well as a reduction in cytokine production in surviving cells. Further, cells that retained the ability to produce IFN-γ exhibited a decreased potential for coproduction of TNF-α. Reduced cytokine production was directly correlated with a decrease in the level of mRNA. Negative regulation of cells in the mediastinal lymph node was minimal compared with that present in the lung, supporting a model of selective regulation in the tissue harboring high pathogen burden. These results show that entry of a coinfecting pathogen can have profound immunoregulatory effects on an ongoing immune response. Together, these findings reveal a novel dynamic interplay between concurrently infecting pathogens and the adaptive immune system.
Copyright ? 2014 by The American Association of Immunologists, Inc.
PMID:
25311807
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25311807
Coinfection with Streptococcus pneumoniae Negatively Modulates the Size and Composition of the Ongoing Influenza-Specific CD8+ T Cell Response.
Blevins LK1, Wren JT1, Holbrook BC1, Hayward SL1, Swords WE1, Parks GD1, Alexander-Miller MA2.
Author information
Abstract
Infection with influenza A virus can lead to increased susceptibility to subsequent bacterial infection, often with Streptococcus pneumoniae. Given the substantial modification of the lung environment that occurs following pathogen infection, there is significant potential for modulation of immune responses. In this study, we show that infection of mice with influenza virus, followed by the noninvasive EF3030 strain of Streptococcus pneumoniae, leads to a significant decrease in the virus-specific CD8+ T cell response in the lung. Adoptive-transfer studies suggest that this reduction contributes to disease in coinfected animals. The reduced number of lung effector cells in coinfected animals was associated with increased death, as well as a reduction in cytokine production in surviving cells. Further, cells that retained the ability to produce IFN-γ exhibited a decreased potential for coproduction of TNF-α. Reduced cytokine production was directly correlated with a decrease in the level of mRNA. Negative regulation of cells in the mediastinal lymph node was minimal compared with that present in the lung, supporting a model of selective regulation in the tissue harboring high pathogen burden. These results show that entry of a coinfecting pathogen can have profound immunoregulatory effects on an ongoing immune response. Together, these findings reveal a novel dynamic interplay between concurrently infecting pathogens and the adaptive immune system.
Copyright ? 2014 by The American Association of Immunologists, Inc.
PMID:
25311807
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25311807