Purpose:Porphyromonas gingivalis is a key pathogen in periodontitis, involved in systemic diseases. P. gingivalis relies on various survival strategies, including the synthesis of intracellular polyphosphate (polyP), which is synthesized by polyphosphate kinase encoded by the ppk gene. In contrast, exogenous polyP inhibits the growth of various bacteria, including P. gingivalis. This study examines the transcriptional response of the ppk-deficient P. gingivalis mutant (CW120) to stress induced by exogenous polyP, focusing on gene expression changes compared to the parent strain, P. gingivalis 381.

Methods:Both P. gingivalis CW120 and 381 strains were exposed to exogenous polyP, followed by microarray analysis. Differentially expressed genes (DEGs) with more than a 2-fold change were identified and further validated by quantitative reverse transcription-polymerase chain reaction.

Results:Exposure to polyP led to significant transcriptional changes in CW120, with 583 DEGs identified. Notably, genes related to energy metabolism and cell division were downregulated, while ribosomal protein genes were upregulated. Lipopolysaccharide (LPS)-related genes exhibited altered expression in both strains, indicating that these changes are not directly linked to the ppk gene. Since different P. gingivalis LPS isoforms interact with Toll-like receptor 2 (TLR2) and TLR4 in distinct ways, polyP-induced changes in LPS could influence TLR-mediated immune responses, which are linked to inflammation and pain signaling.

Conclusions:The findings highlight the role of polyP in modulating P. gingivalis gene expression, particularly in the ppk-deficient mutant, affecting energy metabolism, cell division, and LPS production. The potential impact of polyP on TLR-mediated immune pathways suggests its role in modulating bacterial virulence and contributing to chronic pain conditions. Future studies should explore these interactions to inform therapeutic strategies targeting P. gingivalis-related diseases.