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Characterization of Inflammatory Responses During Intranasal Colonization with Streptococcus pneumoniae
Published on: January 17, 2014
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.
Abstract:
The interaction between Streptococcus pneumoniae (S. pneumoniae) and the mucosal epithelial cells of its host is a prerequisite for pneumococcal disease development, yet the specificity of this interaction between different respiratory cells is not fully understood. In the present study, three areas were examined: i) The capability of the encapsulated S. pneumoniae serotype 3 strain (WU2) to adhere to and invade primary nasal‑derived epithelial cells in comparison to primary oral‑derived epithelial cells, A549 adenocarcinoma cells and BEAS‑2B viral transformed bronchial cells; ii) the capability of the unencapsulated 3.8DW strain (a WU2 derivative) to adhere to and invade the same cells over time; and iii) the ability of various genetically‑unrelated encapsulated and unencapsulated S. pneumoniae strains to adhere to and invade A549 lung epithelial cells. The results of the present study demonstrated that the encapsulated WU2 strain adhesion to and invasion of primary nasal epithelial cells was greatest, followed by BEAS‑2B, A549 and primary oral epithelial cells. By contrast, the unencapsulated 3.8‑DW strain invaded oral epithelial cells significantly more efficiently when compared to the nasal epithelial cells. In addition, unencapsulated S. pneumoniae strains adhered to and invaded the A459 cells significantly more efficiently than the encapsulated strains; this is consistent with previously published data. In conclusion, the findings presented in the current study indicated that the adhesion and invasion of the WU2 strain to primary nasal epithelial cells was more efficient compared with the other cultured respiratory epithelial cells tested, which corresponds to the natural course of S. pneumoniae infection and disease development. The target cell preference of unencapsulated strains was different from that of the encapsulated strains, which may be due to the exposure of cell wall proteins.
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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