Affiliation:
1. Host-Pathogen Interactions Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland
Abstract
ABSTRACT
Nasal carriage of
Staphylococcus aureus
is a significant risk factor for secondary staphylococcal pneumonia in influenza A virus (IAV)-infected hosts. However, little research has been undertaken to define the environmental and physiological changes that cause
S. aureus
to shift from commensal to pathogenic organism in this setting. The ability of virus-driven danger signals to cause
S. aureus
to transition from commensalism to pulmonary infection was explored in a recent study by Reddinger et al. R. M. Reddinger, N. R. Luke-Marshall, A. P. Hakansson, and A. A. Campagnari, mBio 7(6):e01235-16, 2016,
http://dx.doi.org/10.1128/mBio.01235-16
. The authors report that physiological host changes, including febrile temperature and a combination of host stress response signals, caused
S. aureus
biofilms to disperse from the nasal environment and cause active pulmonary infection. This commentary discusses the new finding in light of the current understanding of the mechanisms behind staphylococcal coinfection with IAV. In addition, it considers the mechanisms behind staphylococcal dispersal in this model. Overall, the study indicates that interkingdom signaling may occur following IAV infection and this likely contributes to sensitizing the IAV-infected host to secondary staphylococcal pneumonia.
Funder
Science Foundation Ireland
Irish Research Council
Publisher
American Society for Microbiology
Cited by
55 articles.
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