Abstract

BackgroundPorphyromonas gingivalis is considered a keystone pathogen responsible for chronic periodontitis. Although several virulence factors produced by this bacterium are quite well characterized, very little is known about regulatory mechanisms that allow different strains of P. gingivalis to efficiently survive in the hostile environment of the oral cavity, a typical habitat characterized by low iron and heme concentrations. The aim of this study was to characterize P. gingivalis Fur homolog (PgFur) in terms of its role in production of virulence factors in more (A7436) and less (ATCC 33277) virulent strains.ResultsExpression of a pgfur depends on the growth phase and iron/heme concentration. To better understand the role played by the PgFur protein in P. gingivalis virulence under low- and high-iron/heme conditions, a pgfur-deficient ATCC 33277 strain (TO16) was constructed and its phenotype compared with that of a pgfur A7436-derived mutant strain (TO6). In contrast to the TO6 strain, the TO16 strain did not differ in the growth rate and hemolytic activity compared with the ATCC 33277 strain. However, both mutant strains were more sensitive to oxidative stress and they demonstrated changes in the production of lysine- (Kgp) and arginine-specific (Rgp) gingipains. In contrast to the wild-type strains, TO6 and TO16 mutant strains produced larger amounts of HmuY protein under high iron/heme conditions. We also demonstrated differences in production of glycoconjugates between the A7436 and ATCC 33277 strains and we found evidence that PgFur protein might regulate glycosylation process. Moreover, we revealed that PgFur protein plays a role in interactions with other periodontopathogens and is important for P. gingivalis infection of THP-1-derived macrophages and survival inside the cells. Deletion of the pgfur gene influences expression of many transcription factors, including two not yet characterized transcription factors from the Crp/Fnr family. We also observed lower expression of the CRISPR/Cas genes.ConclusionsWe show here for the first time that inactivation of the pgfur gene exerts a different influence on the phenotype of the A7436 and ATCC 33277 strains. Our findings further support the hypothesis that PgFur regulates expression of genes encoding surface virulence factors and/or genes involved in their maturation.

Highlights

  • Porphyromonas gingivalis is considered a keystone pathogen responsible for chronic periodontitis

  • In our previous study, we reported preliminary analysis of a pgfur mutant strain (TO6) constructed in the more virulent A7436 wild-type strain [31] and suggested that P. gingivalis ferric uptake regulator (Fur) homolog (PgFur) can influence in vivo P. gingivalis growth and virulence, allowing efficient infection through a complex regulatory network

  • To provide more accurate and deeper understanding of the biological role played by PgFur in the production of virulence factors, we inactivated the P. gingivalis pgfur gene in the less virulent ATCC 33277 strain

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Summary

Introduction

Porphyromonas gingivalis is considered a keystone pathogen responsible for chronic periodontitis. Analyses of subgingival samples revealed the presence and relative abundance of periodontal pathogens, including the “red complex” bacteria (Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola) [3], which are associated with the clinical features of chronic periodontitis [4, 5]. Other bacteria, such as Streptococcus gordonii, a member of the “yellow complex”, and Prevotella intermedia, a member of the “orange complex”, serve as early colonizers or bridging species to members of the “red complex” [3, 6, 7]. The predominant form of Kgp and RgpA is a complex of a catalytic domain with hemagglutinin/adhesion domains

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