Host Physiologic Changes Induced by Influenza A Virus Lead to Staphylococcus aureus Biofilm Dispersion and Transition from Asymptomatic Colonization to Invasive Disease.
Reddinger RM, Luke-Marshall NR, Hakansson AP, Campagnari AA
MBio. 2016. doi: 10.1128/mBio.01235-16e01235-16
COMMENT: It is well known that after influenza virus infection Staphylococcus aureus can change from asymptomatic colonization to produce an invasive staphylococcal disease being one of the most important cause of secondary pneumonia.
In this article the authors analyze in vitro using S. aureus UAMS-1 on prefixed human respiratory epithelial cell substrata. The results indicates that S. aureus forms biofilms in this situation and they tested if certain signals associated to Influenza virus infection were able to change this behaviour.
Elevated temperature led to fourfold-higher dispersal of S. aureus from the biofilm than in controls.
Then, they tested in vivo in mice and found that UAMS-1 stably colonizes the murine nasal mucosa for 48 h in biofilms, and in some cases for 1 week, without detectable dissemination into the lungs or development of invasive disease however mice exposed to febrile-range temperatures had high levels of UAMS-1 in the lungs. Finally, they anlyzed if influenza A virus infection elicited secondary staphylococcal pneumonia using their mouse colonization model. influenza virus infection in mice asymptomatically colonized with UAMS-1 in their nasal tissues induced a transition from colonization to invasive disease and causes pronounced secondary staphylococcal pneumonia.
In summary it is a very interesting paper providing new insights on the viral / bacterial interplay in the natural history of infections.