Host physiologic changes induced by influenza a virus lead to staphylococcus aureus biofilm dispersion and transition from asymptomatic colonization to invasive disease
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UNLABELLED: Staphylococcus aureus is a ubiquitous opportunistic human pathogen and a major health concern worldwide, causing a wide variety of diseases from mild skin infections to systemic disease. S. aureus is a major source of severe secondary bacterial pneumonia after influenza A virus infection, which causes widespread morbidity and mortality. While the phenomenon of secondary bacterial pneumonia is well established, the mechanisms behind the transition from asymptomatic colonization to invasive staphylococcal disease following viral infection remains unknown. In this report, we have shown that S. aureus biofilms, grown on an upper respiratory epithelial substratum, disperse in response to host physiologic changes related to viral infection, such as febrile range temperatures, exogenous ATP, norepinephrine, and increased glucose. Mice that were colonized with S. aureus and subsequently exposed to these physiologic stimuli or influenza A virus coinfection developed pronounced pneumonia. This study provides novel insight into the transition from colonization to invasive disease, providing a better understanding of the events involved in the pathogenesis of secondary staphylococcal pneumonia. IMPORTANCE: In this study, we have determined that host physiologic changes related to influenza A virus infection causes S. aureus to disperse from a biofilm state. Additionally, we report that these same host physiologic changes promote S. aureus dissemination from the nasal tissue to the lungs in an animal model. Furthermore, this study identifies important aspects involved in the transition of S. aureus from asymptomatic colonization to pneumonia.
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Viruses impair bacterial biofilm formation and disrupt existing biofilm.
“Viruses have also been found to impair bacterial biofilm formation and disrupt existing biofilm (141–144).”
From Respiratory viral infection-induced microbiome alterations and secondary bacterial pneumonia. (2018) · cites this paper as [141]
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- Authors
- Reddinger, R. M., Luke-Marshall, N. R., Hakansson, A. P., & Campagnari, A. A.
- Affiliations
- University at Buffalo, State University of New York (US)
- Department of Microbiology and Immunology, University at Buffalo, State University of New York, Buffalo, New York, USA
- Corresponding author
- Campagnari, Anthony A.
- Venue
- mBio
- Publisher
- American Society for Microbiology
- Published
- 2016-09-07
- Volume
- 7
- Issue
- 4
- ISSN
- 2150-7511 (ISSN-L)
- 2161-2129
- PMC
- PMC4981728
- OpenAlex
- W2480595178
- Cited by
- 62
- References
- 67
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 2 · 2023: 4 · 2022: 8 · 2021: 7 · 2020: 10 · 2019: 7 · 2018: 12 · 2017: 3 · 2016: 1
- FWCI
- 3.98
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- mBio (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- HHS | NIH | National Institute on Deafness and Other Communication Disorders (R01DC013554)
- Vetenskapsrådet (2015-03704)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bacterial biofilms and quorum sensing
- Health Sciences › Medicine › Infectious Diseases › Antimicrobial Resistance in Staphylococcus
- Life Sciences › Immunology and Microbiology › Microbiology › Microbial infections and disease research
- Keywords
- Staphylococcus aureus, influenza A virus, biofilm dispersal, secondary bacterial pneumonia, staphylococcal colonization, fever, ATP, norepinephrine, glucose, co-infection
- MeSH terms
- Animals, Cell Line, Disease Models, Animal, Epithelial Cells, Humans, Mice, Inbred BALB C, Orthomyxoviridae Infections, Influenza A virus, Pneumonia, Staphylococcal, Staphylococcus aureus, Biofilms, Host-Pathogen Interactions
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