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Using Bioluminescent Imaging to Investigate Synergism Between Streptococcus pneumoniae and Influenza A Virus in Infant Mice
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Using Bioluminescent Imaging to Investigate Synergism Between Streptococcus pneumoniae and Influenza A Virus in Infant Mice

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Double-Edged Role of Interleukin 17A in Streptococcus pneumoniae Pathogenesis During Influenza Virus Coinfection

Ganesh Ambigapathy1, Taylor Schmit1, Ram Kumar Mathur2

  • 1Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks.

The Journal of Infectious Diseases
|June 12, 2019
PubMed
Abstract

Insights

Host interleukin 17A (IL-17A) response initially limits Streptococcus pneumoniae colonization. However, during influenza A virus coinfection, IL-17A exacerbates pneumococcal disease in the nasopharynx.

Area of Science:

  • Immunology
  • Microbiology
  • Infectious Diseases

Background:

  • Streptococcus pneumoniae colonization can transition to invasive disease.
  • Influenza virus coinfection complicates bacterial pathogenesis.
  • The role of interleukin 17A (IL-17A) in this context is not fully understood.

Purpose of the Study:

  • To investigate the host IL-17A response to S. pneumoniae colonization.
  • To determine how influenza A virus coinfection alters the IL-17A response and S. pneumoniae pathogenesis.
  • To elucidate the role of IL-17A in S. pneumoniae colonization and influenza virus coinfection.

Main Methods:

  • Used wild-type (WT) and genetically modified mice (RoRγt-/-, RAG1-/-).
  • Administered S. pneumoniae serotype 6A for colonization, followed by influenza A virus (PR8) infection.
  • Employed antibody-mediated depletion of IL-17A and CD90+ cells.

Main Results:

  • IL-17A neutralization impaired S. pneumoniae clearance in WT mice.
  • RAG1-/- mice failed to clear S. pneumoniae colonization; CD90+ cell depletion reduced invasion.
  • Coinfection induced a strong IL-17A response, increasing S. pneumoniae invasive disease, which was reduced by IL-17A neutralization and in RoRγt-/- mice.

Conclusions:

  • IL-17A plays a dual role: limiting S. pneumoniae colonization but promoting disease during influenza coinfection.
  • Influenza virus coinfection triggers a pro-inflammatory IL-17A response that enhances S. pneumoniae pathogenesis in the nasopharynx.
Keywords:
Streptococcus pneumoniaeIL17Acoinfectionhost responseinfluenza

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