Adhesion and invasion of Streptococcus pneumoniae to primary and secondary respiratory epithelial cells

Sara Novick1, Marilous Shagan1, Karin Blau1

  • 1Shraga Segal Department of Microbiology and Immunology, Faculty of Health Sciences, Ben‑Gurion University of The Negev, Beer Sheva 84101, Israel.

Insights

Streptococcus pneumoniae adhesion and invasion vary by cell type. Encapsulated strains prefer nasal cells, while unencapsulated strains target oral cells, impacting pneumococcal disease development.

Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Host-pathogen interactions are crucial for disease development.
  • The specific interactions between Streptococcus pneumoniae and various respiratory epithelial cells are not fully understood.

Purpose of the Study:

  • To investigate the adherence and invasion capabilities of encapsulated and unencapsulated Streptococcus pneumoniae strains on different respiratory cell types.
  • To compare the tropism of encapsulated versus unencapsulated S. pneumoniae strains.

Main Methods:

  • Comparative analysis of S. pneumoniae (serotype 3, WU2 strain) adherence and invasion on primary nasal, oral, A549, and BEAS-2B cells.
  • Time-dependent assessment of an unencapsulated strain (3.8DW) on these cell types.
  • Evaluation of various S. pneumoniae strains on A549 lung epithelial cells.

Main Results:

  • The encapsulated WU2 strain showed greatest adhesion and invasion in primary nasal epithelial cells, followed by BEAS-2B, A549, and primary oral cells.
  • The unencapsulated 3.8DW strain invaded oral epithelial cells more efficiently than nasal cells.
  • Unencapsulated S. pneumoniae strains demonstrated significantly higher adherence and invasion in A549 cells compared to encapsulated strains.

Conclusions:

  • Encapsulated S. pneumoniae (WU2) preferentially adheres to and invades primary nasal epithelial cells, aligning with natural infection patterns.
  • Unencapsulated S. pneumoniae strains exhibit different cell tropism, potentially due to exposed cell wall proteins.
  • Understanding these specific interactions is key to comprehending pneumococcal disease pathogenesis.

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