Open AccessInfluenza A virus‐mediated priming enhances cytokine secretion by human dendritic cells infected with S treptococcus pneumoniae
Author(s) -
Kuri Thomas,
Smed Sörensen Anna,
Thomas Saskia,
Karlsson Hedestam Gunilla B.,
Normark Staffan,
HenriquesNormark Birgitta,
McInerney Gerald M.,
Plant Laura
Publication year - 2013
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12122
Subject(s) - biology , influenza a virus , microbiology and biotechnology , priming (agriculture) , streptococcus pneumoniae , immune system , cytokine , immunology , secretion , virus , pathogen , dendritic cell , virology , antibiotics , biochemistry , botany , germination
Summary Secondary infections with S treptococcus 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 analysed 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.