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Cited by 233Influenza Virus Research StudiesNeutrophil, Myeloperoxidase and Oxidative MechanismsPneumonia and Respiratory Infections

Both Influenza-Induced Neutrophil Dysfunction and Neutrophil-Independent Mechanisms Contribute to Increased Susceptibility to a Secondary Streptococcus pneumoniae Infection

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McNamee, Lynnelle A., Harmsen, Allen G.·2006·Infection and Immunity
DOI 10.1128/iai.00789-06PMC PMC1698099
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Abstract

Since secondary Streptococcus pneumoniae infections greatly increase the mortality of influenza infections, we determined the relative roles of neutrophil-dependent and -independent mechanisms in increased susceptibility to S. pneumoniae during influenza infection. Mice infected with influenza for 6 days, but not 3 days, showed a significant increase in susceptibility to S. pneumoniae infection compared to mice not infected with influenza. There was significant neutrophil accumulation in the lungs of S. pneumoniae-infected mice regardless of whether or not they were infected with influenza for 3 or 6 days. Depletion of neutrophils in these mice resulted in increased susceptibility to S. pneumoniae in both the non-influenza-infected mice and mice infected with influenza for 3 days but not in the mice infected with influenza for 6 days, indicating that a prior influenza infection of 6 days may compromise neutrophil function, resulting in increased susceptibility to a S. pneumoniae infection. Neutrophils from the lungs of mice infected with influenza for 3 or 6 days exhibited functional impairment in the form of decreased phagocytosis and intracellular reactive oxygen species generation in response to S. pneumoniae. In addition, neutrophil-depleted mice infected with influenza for 6 days were more susceptible to S. pneumoniae than neutrophil-depleted mice not infected with influenza, indicating that neutrophil-independent mechanisms also contribute to influenza-induced increased susceptibility to S. pneumoniae. Pulmonary interleukin-10 levels were increased in coinfected mice infected with influenza for 6 days but not 3 days. Thus, an influenza infection of 6 days increases susceptibility to S. pneumoniae by both suppression of neutrophil function and by neutrophil-independent mechanisms such as enhanced cytokine production.

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  • Respiratory viral infections impair innate immune responses against bacteria.

    “Third, respiratory viral infections impair innate immune responses against bacteria (128–130).”

    From Respiratory viral infection-induced microbiome alterations and secondary bacterial pneumonia. (2018) · cites this paper as [130]

  • There seems to be a biphasic response to the virus that alters innate responses to the secondary bacterial pathogen.

    “There seems to be biphasic response to the virus that alters innate responses to the secondary bacterial pathogen.”

    From Influenza virus primes mice for pneumonia from Staphylococcus aureus. (2011) · cites this paper as [43]

  • Roughly 3-10 days after viral infection, a proinflammatory state characterized by granulocyte and monocyte influx into the lungs amplifies host responses to bacteria, resulting in poor outcomes.

    “Roughly 3-10 days after viral infection, a proinflammatory state characterized by granulocyte and monocyte influx into the lungs amplifies host responses to bacteria, resulting in poor outcomes [23,25,43].”

    From Influenza virus primes mice for pneumonia from Staphylococcus aureus. (2011) · cites this paper as [43]

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Authors
McNamee, L. A., & Harmsen, A. G.
Affiliations
Montana State University (US)
Corresponding author
McNamee, Lynnelle A.
Venue
Infection and Immunity
Publisher
American Society for Microbiology
Published
2006-12
Volume
74
Issue
12
Pages
6707-6721
ISSN
  • 0019-9567 (ISSN-L)
  • 1098-5522
DOI
10.1128/iai.00789-06
PMC
PMC1698099
OpenAlex
W2095929174
Cited by
233
References
69
Citations by year
2026: 4 · 2025: 9 · 2024: 10 · 2023: 8 · 2022: 13 · 2021: 20 · 2020: 23 · 2019: 14 · 2018: 12 · 2017: 7 · 2016: 17 · 2015: 13 · 2014: 17 · 2013: 16 · 2012: 9
FWCI
4.39
Type
journal article
Language
en
Open access
Licence
journals.asm.org/non-commercial-tdm-license (tdm)
Locations
  • Infection and Immunity (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Badan Riset dan Inovasi Nasional
  • National Institutes of Health
  • National Center for Research Resources (P20 RR16455-04, P20RR020185, P20RR016455)
Topics
  • Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Health Sciences › Medicine › Epidemiology › Pneumonia and Respiratory Infections
Keywords
influenza, Streptococcus pneumoniae, secondary bacterial infection, neutrophil dysfunction, neutrophil depletion, phagocytosis, reactive oxygen species, IL-10, bacterial co-infection, host susceptibility
MeSH terms
Animals, Disease Susceptibility, Female, Leukocyte Disorders, Lung, Mice, Inbred C57BL, Neutrophils, Orthomyxoviridae Infections, Pneumonia, Pneumococcal, Streptococcus pneumoniae, Cytokines, Reactive Oxygen Species, Mice

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