ArticlemBio2016
Staphylococcus aureus and Influenza A Virus: Partners in Coinfection.
Article in mBio, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Respiratory Microbiome Remodeling in Aging: Implications for Immunosenescence and Therapeutic Intervention.Immune network · 2026Review
- Host, Pathogen, and Pulmonary Anatomy in Pneumonia: An Integrated Imaging and Clinical Perspective.Diagnostics (Basel, Switzerland) · 2026Review
- Influenza A/PR8 virus infection in mice suppresses basal and Oncostatin M-induced IL-33 expression in vivo and in vitro.Scientific reports · 2026Article
- Microbiological findings and antibiotic treatment in community-acquired pneumonia: a retrospective cohort study.BMC infectious diseases · 2026Article
- Addition of lactoferrin increases efficacy of three Kayviruses and limits the inflammatory response in pulmonary epithelial cells.Applied microbiology and biotechnology · 2026Article
- Co-infection models ofFrontiers in cellular and infection microbiology · 2026Article
- Article
- Correlation between the severity of COVID-19 infection and the presence of oropharyngeal candidiasis: a cross-sectional study in Al-Diwaniyah Hospital, Iraq.The Pan African medical journal · 2025Article
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- Severe Human Parainfluenza Virus Community- and Healthcare-Acquired Pneumonia in Adults at Tertiary Hospital, Seoul, South Korea, 2010-2019.Emerging infectious diseases · 2024Review
- Mortality, incidence, and microbiological documentation of ventilated acquired pneumonia (VAP) in critically ill patients with COVID-19 or influenza.Annals of intensive care · 2023Article
- The Activation of the RIG-I/MDA5 Signaling Pathway upon Influenza D Virus Infection Impairs the Pulmonary Proinflammatory Response Triggered by Mycoplasma bovis Superinfection.Journal of virology · 2023Article
- Microbial and Immune Regulation of the Gut-Lung Axis during Viral-Bacterial Coinfection.Journal of bacteriology · 2023Review
- Specialized pro-resolving lipid mediators regulate inflammatory macrophages: A paradigm shift from antibiotics to immunotherapy for mitigating COVID-19 pandemic.Frontiers in molecular biosciences · 2023Review
- Biogenic silver nanoparticles eradicate ofFrontiers in microbiology · 2023Article
- Microbiological findings and prescribing trends in SARS- CoV-2 positive patients in two United Kingdom Hospitals.Infection prevention in practice · 2022Article
- Essential Fitness Repertoire of Staphylococcus aureus during Co-infection with Acinetobacter baumanniimSystems · 2022Article
- The changing spectrum of microbial aetiology of respiratory tract infections in hospitalized patients before and during the COVID-19 pandemic.BMC infectious diseases · 2022Article
- Oropharyngeal Candidiasis among Egyptian COVID-19 Patients: Clinical Characteristics, Species Identification, and Antifungal Susceptibility, with Disease Severity and Fungal Coinfection Prediction Models.Diagnostics (Basel, Switzerland) · 2022Article
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2 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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