Inherently and Conditionally Essential Protein Catabolism Genes of Porphyromonas gingivalis

Liu

Journal of Periodontology

et al. 2021

Background: Porphyromonas gingivalis (P. gingivalis) and Fusobacterium nucleatum (F. nucleatum) participate in the formation and progression of periodontitis. They can exert virulence by invading into host cells, but the interaction between them and their specific mechanisms remain unclear. The purpose of this study was to study the effect of P. gingivalis outer membrane vesicles (OMVs) on the ability of F. nucleatum to invade oral epithelial cells, and the reasons for the influence. Methods: The invasion abilities of the two bacteria were detected separately after mixed infection of P. gingivalis and F. nucleatum. Next, P. gingivalis OMVs were extracted with the kit, and their influence on the invasion ability of F. nucleatum was tested. The effects of P. gingivalis OMVs on F. nucleatum were evaluated by assessment of bacterial morphology, growth curves, autoaggregation morphology, and the expression of adhesion-related proteins FadA and FomA. Results: Our results showed that P. gingivalis inhibited the invasion of F. nucleatum into oral epithelial cells but F. nucleatum promoted the invasion of P. gingivalis. In subsequent experiments, we extracted P. gingivalis OMVs successfully and revealed that proteases in P. gingivalis OMVs inhibited the invasion of F. nucleatum into oral epithelial cells. Furthermore, P. gingivalis OMVs did not affect the morphology and proliferation of F. nucleatum, but proteases inside decreased the auto-aggregation of F. nucleatum. Additionally, proteases in P. gingivalis OMVs reduced the expression levels of F. nucleatum surface adhesionrelated proteins FadA and FomA. Conclusion: Our study demonstrated that proteases in P. gingivalis OMVs inhibited the invasion of F. nucleatum into oral epithelial cells by downregulating FadA and FomA.

Section: Discussionmentioning

confidence: 99%

“…Studies have confirmed that P. gingivalis and F. nucleatum utilize different invasion strategies 33 . P. gingivalis utilizes the endocytic pathway and lipid rafts to invade host cells 34,35 . F. nucleatum invades host cells through a “zipper” mechanism that relies on a large number of adhesins 36 …”

Section: Discussionmentioning

confidence: 99%

Porphyromonas gingivalis outer membrane vesicles inhibit the invasion of Fusobacterium nucleatum into oral epithelial cells by downregulating FadA and FomA

Liu

Journal of Periodontology

et al. 2021

Front. Cell. Infect. Microbiol.

“…Periodontitis, a common microbiome-driven inflammatory disease ( Hajishengallis, 2022 ), was highly related to H. pylori infection. P. gingivalis , as an established pathogenic agent of periodontitis ( Miller and Scott, 2021 ), had a positive correlation with H. pylori . In chronic periodontitis patients with H. pylori infection, the red complex associated with periodontal disease was significantly increased in plaque, including P. gingivalis, Treponema denticola, Tannerella forsythia ( Hu et al., 2016 ), indicating that H. pylori infection may promote periodontal disease.…”

Section: Helicobacter Pylori and Oral Microbiomementioning

confidence: 99%

The interactions between oral-gut axis microbiota and Helicobacter pylori

Chen

Wang

et al. 2022

In the human body, each microbial habitat exhibits a different microbial population pattern, and these distinctive microflorae are highly related to the development of diseases. The microbial interactions from host different niches are becoming crucial regulators to shape the microbiota and their physiological or pathological functions. The oral cavity and gut are the most complex and interdependent microbial habitats. Helicobacter pylori is one of the most important pathogens from digestive tract, especially the stomach, due to its direct relationships with many gastric diseases including gastric cancer. H. pylori infections can destroy the normal gastric environment and make the stomach a livable channel to enhance the microbial interactions between oral cavity and gut, thus reshaping the oral and gut microbiomes. H. pylori can be also detected in the oral and gut, while the interaction between the oral-gut axis microbiota and H. pylori plays a major role in H. pylori’s colonization, infection, and pathogenicity. Both the infection and eradication of H. pylori and its interaction with oral-gut axis microbiota can alter the balance of the microecology of the oral-gut axis, which can affect the occurrence and progress of related diseases. The shift of oral-gut axis microbiota and their interactions with H. pylori maybe potential targets for H. pylori infectious diagnosis and treatment.

Molecular Oral Microbiology

“…The authors argued that an affiliated reduction in ragA and ragB gene activity implicates RagA and B as essential for growth. It should be noted, however, that transposon sequencing interrogation by several laboratories has not identified ragA or ragB as inherently or conditionally essential (Hutcherson, Gogeneni, et al., 2015; Klein et al., 2012, 2017; Miller et al., 2017; Miller & Scott, 2021; Naito et al., 2019).…”

Section: Rag Proteins As Therapeutic Targets For Periodontal Diseasementioning

confidence: 99%

The RagA and RagB proteins of Porphyromonas gingivalis

Potempa

Madej

Scott

2021

Self Cite

RagA and RagB proteins are major components of the outer membrane of the oral pathogen Porphyromonas gingivalis and, while recently suggested to represent a novel peptide uptake system, their full function is still under investigation. Herein, we (a) discuss the evidence that the rag locus contributes to P. gingivalis virulence; (b) provide insight to Rag protein potential biological function in macromolecular transport and other aspects of bacterial physiology; (c) address the host response to Rag proteins which are immunodominant and immunomodulatory; and (d) review the potential of Rag‐focused therapeutic strategies for the control of periodontal diseases.