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Influenza A virus-mediated priming enhances cytokine secretion by human dendritic cells infected with Streptococcus pneumoniae

tetano

Editor, Senior Moderator
Cell Microbiol. 2013 Feb 20. doi: 10.1111/cmi.12122. [Epub ahead of print]
Influenza A virus-mediated priming enhances cytokine secretion by human dendritic cells infected with Streptococcus pneumoniae.
Kuri T, Smed S?rensen A, Thomas S, Karlsson Hedestam GB, Normark S, Henriques-Normark B, McInerney GM, Plant L.
Source

Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Nobels v?g 16, Stockholm, SE-171 77, Sweden; Department of Laboratory Medicine, Division of Clinical Microbiology, Karolinska University Hospital, Stockholm, SE-171 76, Sweden.
Abstract

Secondary infections with Streptococcus pneumoniae (SP) are frequently observed following influenza A virus (IAV) infection and have a substantial impact on global health. Despite this, the basis for the disease progression is incompletely understood. To investigate the effect of co-infection on human monocyte-derived dendritic cells (MDDCs) we analyzed the expression of clinically important pro-inflammatory and immune-modulatory cytokines. IAV infection or treatment with supernatants from IAV-infected cell cultures resulted in priming of the DCs which subsequently influenced the production of IL-12p70, as well as IL-6, following SP infection. Co-infection of the same cell was not required but this effect was dependent on the time, dose and duration of the infections, as well as pathogen viability, bacterial uptake and endosome acidification. Bacterially infected cells were characterized as the main producers of IL-12p70. Finally, we showed that type I interferons were primarily responsible for the priming of IL-12p70 that was observed by infection with IAV. These results provide a probable mechanism for the elevated levels of particular cytokines observed in IAV and SP co-infected cell cultures with implications for the pathogenic outcome observed during in vivo infection.

? 2013 Blackwell Publishing Ltd.

PMID:
23421931
[PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/23421931
 
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