The oral-respiratory interface: modulation of Streptococcus pneumoniae serotype adhesion by the periodontal pathogen Porphyromonas gingivalis W83

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.