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Investigating the Effects of Probiotics on Pneumococcal Colonization Using an In Vitro Adherence Assay
Published on: April 28, 2014
The oral-respiratory interface: modulation of Streptococcus pneumoniae serotype adhesion by the periodontal pathogen
Chrysanti Murad1, Yasmin Hanifa Salma2,3, Imam Megantara1
1Department of Biomedical Sciences, Faculty of Medicine, Universitas Padjadjaran, Bandung, Indonesia.
Background:
Porphyromonas gingivalis, a keystone periodontal pathogen synergizes with Streptococcus pneumoniae by upregulating host receptors like the platelet-activating factor receptor (PAFR). This study investigated whether P. gingivalis W83 differentially modulates the adhesion of four pneumococcal serotypes (3, 4, 6A, and 7F) to alveolar epithelial cells, hypothesizing a strictly serotype-dependent synergy.
Methods:
An in vitro model used A549 alveolar epithelial cells conditioned with P. gingivalis W83 supernatant (PgSup) for 24 h. PAFR upregulation was verified via RT-qPCR. Cells were subsequently infected with the specified pneumococcal serotypes. Adhesion was quantified by colony-forming unit (CFU) counts and analyzed via one-way ANOVA.
Results:
PgSup significantly upregulated PAFR mRNA expression (p < 0.05). This priming associated with a serotype-dependent enhancement of bacterial adhesion. Serotypes 4 (p = 0.022; 95% CI [3260]-[25273]; Cohen's d = 2.94) and 7F (p = 0.017; 95% CI [767.6]-[4432]; Cohen's d = 3.22) demonstrated significant increases in epithelial attachment. Conversely, thickly encapsulated serotypes 3 and 6A exhibited non-significant adhesion increases (p > 0.05).
Conclusion:
P. gingivalis W83 modifies the pulmonary epithelium to favor specific pneumococcal serotypes, an effect temporally associated with host PAFR transcriptional upregulation. These findings highlight a critical oral-respiratory synergy defining host susceptibility to pneumonia.
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