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A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness
12:21

A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness

Published on: September 28, 2022

Involvement of the platelet-activating factor receptor in host defense against Streptococcus pneumoniae during

Koenraad F van der Sluijs1, Leontine J R van Elden, Monique Nijhuis

  • 1Laboratory of Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. kvandersluijs@amc.uva.nl

American Journal of Physiology. Lung Cellular and Molecular Physiology
|August 16, 2005
PubMed

Insights

Platelet-activating factor receptor (PAFR) plays a key role in severe pneumonia following influenza A infection. Blocking PAFR in mice significantly reduced bacterial growth and improved survival after secondary Streptococcus pneumoniae infection.

Area of Science:

  • Immunology
  • Microbiology
  • Pathology

Background:

  • Secondary bacterial pneumonia is a common complication of influenza.
  • Streptococcus pneumoniae is a frequent cause of post-influenza pneumonia.
  • Streptococcus pneumoniae uses the platelet-activating factor receptor (PAFR) to invade respiratory cells, which is upregulated during viral infections.

Purpose of the Study:

  • To investigate the role of PAFR in post-influenza pneumococcal pneumonia using PAFR gene-deficient (PAFR-/-) mice.

Main Methods:

  • Comparison of viral clearance, bacterial outgrowth, infection dissemination, survival rates, and pulmonary cytokine levels between wild-type and PAFR-/- mice after sequential influenza A and Streptococcus pneumoniae infections.

Main Results:

  • Viral clearance was comparable between wild-type and PAFR-/- mice.
  • PAFR-/- mice showed significantly reduced bacterial outgrowth and infection dissemination.
  • PAFR-/- mice exhibited prolonged survival and lower pulmonary levels of IL-10 and KC.

Conclusions:

  • The platelet-activating factor receptor (PAFR) is utilized by Streptococcus pneumoniae during secondary pneumonia following influenza A infection.
  • Targeting PAFR may offer a therapeutic strategy to mitigate severe outcomes of post-influenza bacterial pneumonia.

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