Role of the Porphyromonas gingivalis iron-binding protein PG1777 in oxidative stress resistance

McKenzie, Rachelle M E; Henry, Leroy G.; Boutrin, Marie‐Claire; Ximinies, Alexia; Fletcher, Hansel M.

doi:10.1099/mic.0.000213

Cited by 10 publications

(12 citation statements)

References 38 publications

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“…Surprisingly, these anaerobic pathogens, including P. gingivalis , have also been reported in supragingival plaque, saliva and mucosa samples 9 , 10 , which are thought to be more micro-aerobic environments in the oral cavity. Several proteins have been reported to participate in the resistance to oxidative stress in P. gingivalis 11 – 14 and they may promote the survival of P. gingivalis under micro-aerobic conditions.…”

Section: Introductionmentioning

confidence: 99%

Aggregatibacter actinomycetemcomitans mediates protection of Porphyromonas gingivalis from Streptococcus sanguinis hydrogen peroxide production in multi-species biofilms

Zhu

MacLeod

Newsome

et al. 2019

Sci Rep

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Mixed species biofilms are shaped and influenced by interactions between species. In the oral cavity, dysbiosis of the microbiome leads to diseases such as periodontitis. Porphyromonas gingivalis is a keystone pathogen of periodontitis. In this study, we showed that polymicrobial biofilm formation promoted the tolerance of Porphyromonas gingivalis to oxidative stress under micro-aerobic conditions. The presence of Streptococcus sanguinis, an oral commensal bacterium, inhibited the survival of P. gingivalis in dual-species biofilms via the secretion of hydrogen peroxide (H2O2). Interestingly, this repression could be attenuated by the presence of Aggregatibacter actinomycetemcomitans in tri-species biofilms. It was also shown that the katA gene, encoding a cytoplasmic catalase in A. actinomycetemcomitans, was responsible for the reduction of H2O2 produced by S. sanguinis, which consequently increased the biomass of P. gingivalis in tri-species biofilms. Collectively, these findings reveal that polymicrobial interactions play important roles in shaping bacterial community in biofilm. The existence of catalase producers may support the colonization of pathogens vulnerable to H2O2, in the oral cavity. The catalase may be a potential drug target to aid in the prevention of periodontitis.

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Section: Introductionmentioning

confidence: 99%

Aggregatibacter actinomycetemcomitans mediates protection of Porphyromonas gingivalis from Streptococcus sanguinis hydrogen peroxide production in multi-species biofilms

Zhu

MacLeod

Newsome

et al. 2019

Sci Rep

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“…Porphyromonas gingivalis wild‐type strain, W83 , was used for this study and grown as previously described (McKenzie et al., 2016). Briefly, P. gingivalis was first streaked onto BHI agar supplemented with 5% (v/v) sheep blood and incubated at 37°C for 5–7 days under anaerobic conditions (10% H 2 , 10% CO 2 , 80% N 2 ).…”

Section: Methodsmentioning

confidence: 99%

“…Porphyromonas gingivalis wild-type strain, W83, was used for this study and grown as previously described (McKenzie et al, 2016).…”

Section: Bacterial Growth Conditionsmentioning

confidence: 99%

Platelet plug formation in whole blood is enhanced in the presence of Porphyromonas gingivalis

Chen

Fletcher

Gheorghe

et al. 2020

Molecular Oral Microbiology

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Hemostasis involves a highly regulated equilibrium between pro and anticoagulant processes. It is a dynamic system comprising cellular and plasma factors that interact with damaged vascular tissue to minimize blood loss. Platelets are anucleate cellular fragments derived from mature megakaryocytes via a process called thrombopoiesis (Stegner et al., 2017). They circulate throughout the vascular system in a quiescent discoid form, interacting minimally with healthy endothelial cells. Following injury to the endothelium, platelets serve as key effector cells for the hemostatic response. They rapidly adhere to exposed extracellular matrix via tether receptor complexes such as collagen-glycoprotein (GP) VI and von Willebrand factor-GPIb-V-IX (Canobbio et al., 2004; Chen et al., 2002). Platelet attachment triggers downstream effects including the release of platelet-specific α granules and dense granules (Blair & Flaumenhaft, 2009; Li et al., 2010). Contained within these granules are important membrane bound receptors (GPIIb/IIIa and P-selectin), platelet mediators (adenosine 5ʹ-diphosphate [ADP] and calcium ions; Blair et al., 2009; Sharda & Flaumenhaft, 2018). Release of ADP, a potent platelet agonist, is crucial for the formation of an effective platelet plug. Such ADP mediated activation leads to morphological changes, transforming resting discoid platelets to an amoeboid state with numerous pseudopodia that facilitate platelet interdigitation and stabilize the developing aggregate

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“…A recent study reported that P. gingivalis iron-binding protein PG1777 was associated with resistance to oxidative stress (McKenzie et al, 2016). Under prolonged oxidative stress, the expression of a unique gene cluster grpE-dnaJ-PG1777-PG1778-PG1779 increased in P. gingivalis, and the recombinant PG1777 protein exhibited iron-binding properties and protected DNA from degradation.…”

Section: Resistance To Ros-mediated Killingmentioning

confidence: 99%

Interactions Between Neutrophils and Periodontal Pathogens in Late-Onset Periodontitis

Jiang

Zhao

Shui

et al. 2021

Front. Cell. Infect. Microbiol.

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Late-onset periodontitis is associated with a series of inflammatory reactions induced by periodontal pathogens, such as Porphyromonas gingivalis, a keystone pathogen involved in periodontitis. Neutrophils are the most abundant leukocytes in the periodontal pocket/gingival crevice and inflamed periodontal tissues. They form a “wall” between the dental plaque and the junctional epithelium, preventing microbial invasion. The balance between neutrophils and the microbial community is essential to periodontal homeostasis. Excessive activation of neutrophils in response to periodontal pathogens can induce tissue damage and lead to periodontitis persistence. Therefore, illuminating the interactions between neutrophils and periodontal pathogens is critical for progress in the field of periodontitis. The present review aimed to summarize the interactions between neutrophils and periodontal pathogens in late-onset periodontitis, including neutrophil recruitment, neutrophil mechanisms to clear the pathogens, and pathogen strategies to evade neutrophil-mediated elimination of bacteria. The recruitment is a multi-step process, including tethering and rolling, adhesion, crawling, and transmigration. Neutrophils clear the pathogens mainly by phagocytosis, respiratory burst responses, degranulation, and neutrophil extracellular trap (NET) formation. The mechanisms that pathogens activate to evade neutrophil-mediated killing include impairing neutrophil recruitment, preventing phagocytosis, uncoupling killing from inflammation, and resistance to ROS, degranulation products, and NETs.

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Role of the Porphyromonas gingivalis iron-binding protein PG1777 in oxidative stress resistance

Cited by 10 publications

References 38 publications

Aggregatibacter actinomycetemcomitans mediates protection of Porphyromonas gingivalis from Streptococcus sanguinis hydrogen peroxide production in multi-species biofilms

Aggregatibacter actinomycetemcomitans mediates protection of Porphyromonas gingivalis from Streptococcus sanguinis hydrogen peroxide production in multi-species biofilms

Platelet plug formation in whole blood is enhanced in the presence of Porphyromonas gingivalis

Interactions Between Neutrophils and Periodontal Pathogens in Late-Onset Periodontitis

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