Staphylococcus aureus and Influenza A Virus: Partners in Coinfection
Michelle E Mulcahy1, Rachel M McLoughlin2
1Host-Pathogen Interactions Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
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.
Insights
Influenza A virus infection causes host physiological changes, like fever, that promote Staphylococcus aureus nasal biofilms to disperse and cause pneumonia. This highlights interkingdom signaling in secondary bacterial infections.
Area of Science:
- Microbiology
- Immunology
- Virology
Background:
- Nasal carriage of Staphylococcus aureus is a major risk factor for secondary pneumonia in influenza A virus (IAV)-infected individuals.
- Limited research exists on the environmental and physiological triggers for S. aureus transitioning from commensal to pathogenic states during IAV infection.
Purpose of the Study:
- To investigate how virus-induced danger signals and host physiological changes promote S. aureus transition from commensalism to pulmonary infection.
- To explore the mechanisms of S. aureus dispersal from the nasal environment during IAV infection.
Main Methods:
- The study by Reddinger et al. examined the impact of host physiological changes (febrile temperature, stress signals) on S. aureus behavior.
- Analysis of interkingdom signaling between IAV and S. aureus.
Main Results:
- Host physiological changes, including fever and stress responses, induced S. aureus biofilm dispersal from the nasal cavity.
- Dispersed S. aureus initiated active pulmonary infections, leading to secondary pneumonia.
Conclusions:
- IAV infection creates a host environment conducive to S. aureus pathogenesis.
- Interkingdom signaling between IAV and S. aureus likely sensitizes the host, contributing to secondary staphylococcal pneumonia.
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