Porphyromonas gingivalis (P. gingivalis) is a Gram-negative anaerobic pathogen that is involved in the pathogenesis of periodontitis and systemic diseases. P. gingivalis has recently been detected in rheumatoid arthritis (RA), cardiovascular disease, and tumors, as well as Alzheimer’s disease (AD), and the presence of P. gingivalis in these diseases are correlated with poor prognosis. Macrophages are major innate immune cells which modulate immune responses against pathogens, however, multiple bacteria have evolved abilities to evade or even subvert the macrophages’ immune response, in which subsequently promote the diseases’ initiation and progression. P. gingivalis as a keystone pathogen of periodontitis has received increasing attention for the onset and development of systemic diseases. P. gingivalis induces macrophage polarization and inflammasome activation. It also causes immune response evasion which plays important roles in promoting inflammatory diseases, autoimmune diseases, and tumor development. In this review, we summarize recent discoveries on the interaction of P. gingivalis and macrophages in relevant disease development and progression, such as periodontitis, atherosclerosis, RA, AD, and cancers, aiming to provide an in-depth mechanistic understanding of this interaction and potential therapeutic strategies.
Porphyromonas gingivalis is a keystone pathogen for periodontitis. The function of the GntR family transcription factor is poorly studied in P. gingivalis. Numerous processes govern bacterial growth. The survival and pathogenicity of P. gingivalis depend heavily on its capacity to acquire amino acids as nutritional sources. In this investigation, a GntR transcription factor, pg1007, was identified in P. gingivalis, the deletion of which significantly inhibited bacterial growth. The mutant strain also exhibited an increased extracellular activity of gingipains and acylpeptidyl oligopeptidase (AOP). Global gene expression profiling revealed that the expression levels of 59 genes were significantly altered in the Δpg1007 mutant, with an upregulation in gene expression for AOP, ABC transporters, and some membrane proteins. In addition, His‐PG1007 protein was purified as a recombinant protein from Escherichia coli, and the conserved DNA sequence bound by it was determined using electrophoretic mobility shift assays and DNase I footprinting assays. Consequently, this study demonstrated that pg1007 is a crucial transcription factor in P. gingivalis and regulates the bacterial growth and activity of gingipains and AOP. These findings may enhance our understanding of the regulation of bacterial proliferation and protease activity in P. gingivalis.
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