Dataset Information

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

ABSTRACT:

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, auto-aggregation 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 adhesion-related 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.

SUBMITTER: Zhang Z

PROVIDER: S-EPMC9415117 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature

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Publications

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

Zhang Zhiying Z Liu Sai S Zhang Shuwei S Li Yuchao Y Shi Xiaoting X Liu Dongjuan D Pan Yaping Y

Journal of periodontology 20211005 4

<h4>Background</h4>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.<h4>M ...[more]

PMID: 34458990

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Project description:IntroductionMetastasis is an important cause of high mortality and lethality of oral cancer. Fusobacterium nucleatum (Fn) can promote tumour metastasis. Outer membrane vesicles (OMVs) are secreted by Fn. However, the effects of Fn-derived extracellular vesicles on oral cancer metastasis and the underlying mechanisms are unclear.ObjectivesWe aimed to determine whether and how Fn OMVs mediate oral cancer metastasis.MethodsOMVs were isolated from brain heart infusion (BHI) broth supernatant of Fn by ultracentrifugation. Tumour-bearing mice were treated with Fn OMVs to evaluate the effect of OMVs on cancer metastasis. Transwell assays were performed to determine how Fn OMVs affect cancer cell migration and invasion. The differentially expressed genes in Fn OMV-treated/untreated cancer cells were identified by RNA-seq. Transmission electron microscopy, laser confocal microscopy, and lentiviral transduction were used to detect changes in autophagic flux in cancer cells stimulated with Fn OMVs. Western blotting assay was performed to determine changes in EMT-related marker protein levels in cancer cells. Fn OMVs' effects on migration after blocking autophagic flux by autophagy inhibitors were determined by in vitro and in vivo experiments.ResultsFn OMVs were structurally similar to vesicles. In the in vivo experiment, Fn OMVs promoted lung metastasis in tumour-bearing mice, while chloroquine (CHQ, an autophagy inhibitor) treatment reduced the number of pulmonary metastases resulting from the intratumoral Fn OMV injection. Fn OMVs promoted the migration and invasion of cancer cells in vivo, leading to altered expression levels of EMT-related proteins (E-cadherin downregulation; Vimentin/N-cadherin upregulation). RNA-seq showed that Fn OMVs activate intracellular autophagy pathways. Blocking autophagic flux with CHQ reduced in vitro and in vivo migration of cancer cells induced by Fn OMVs as well as reversed changes in EMT-related protein expression.ConclusionFn OMVs not only induced cancer metastasis but also activated autophagic flux. Blocking autophagic flux weakened Fn OMV-stimulated cancer metastasis.

Dataset Information

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

Background

Methods

Results

Conclusion

Publications

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

Similar Datasets

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