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The involvement of CdhR in Porphyromonas gingivalis during Nitric Oxide stress

ABSTRACT: The involvement of CdhR in Porphyromonas gingivalis during Nitric Oxide stress

PROVIDER: PRJNA929501 | ENA |

REPOSITORIES: ENA

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The involvement of CdhR in Porphyromonas gingivalis during Nitric Oxide stress [microarray]

Project description:The involvement of CdhR in Porphyromonas gingivalis during Nitric Oxide stress [microarray]

| PRJNA929507 | ENA

The involvement of CdhR in Porphyromonas gingivalis during Nitric Oxide stress [RNA-seq]

Project description:The involvement of CdhR in Porphyromonas gingivalis during Nitric Oxide stress [RNA-seq]

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The involvement of CdhR in Porphyromonas gingivalis during Nitric Oxide stress [RNA-seq]

Project description:To understand the role of CdhR and its adjacent gene PG1236 in nitric oxide (NO) stress resistance, isogenic mutants P. gingivalis FLL457 (ΔPG1237::ermF), FLL458 (ΔPG1236::ermF) and FLL459 (ΔPG1236-37::ermF) were made by allelic exchange mutagenesis and their gene expression was studied under control and NO stress conditions. DNA microarray analysis of FLL457 showed that approximately 2% of the genes were up regulated and over 1% of the genes down regulated. Transcriptome analysis of FLL458 and FLL459 under NO stress showed similar modulation patterns in both mutants for a few genes. The PG1236-7 gene cluster seemed to be part of the same transcriptional unit that showed increased expression under NO stress. Recombinant CdhR showed binding activity to the predicted promoter regions of PG1459 and PG0495. Taken together, the data indicate that CdhR may play a role in NO stress resistance and be involved in a regulatory network in P. gingivalis.

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The involvement of CdhR in Porphyromonas gingivalis during Nitric Oxide stress [microarray]

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Project description:Porphyromonas gingivalis is the key etiological pathogen of periodontal disease, a chronic oral inflammatory condition that affects over 14% of the global population. P. gingivalis possesses several potent virulence factors—including gingipains, hemagglutinins, and fimbriae—that drive microbial dysbiosis. To restore homeostasis, nitric oxide (NO) is endogenously produced by immune cells to eliminate the infection[HL1.1], but disease persistence necessitates the use of therapeutic agents. The multiple antibacterial mechanisms of NO minimize the potential for antimicrobial resistance compared to traditional antibiotics, making exogenous NO delivery a potential attractive strategy for combating P. gingivalis. The objective of this study was to evaluate the effect of exogenous NO on the virulence of P. gingivalis, including NO’s capacity to influence biofilm formation and dispersion, invasion of host cells, mitigation of immune response, and gingipain activity and production. Nitric oxide effectively modulated the virulent behavior of P. gingivalis by reducing the pathogen’s ability to form biofilms and invade host cells. Nitric oxide exposure also altered the pathogen’s ability to export gingipains, thereby significantly reducing its pathogenicity. This work highlights the therapeutic potential of exogenous NO to alter periodontal disease through its multimodal effects on the virulence of P. gingivalis.

2026-08-13 | PXD071939 | Pride

Role of PG1626 in Porphyromonas gingivalis ATCC33277

Project description:Wild type Porphyromonas gingivalis strain ATCC33277 (V3176) and PG1626 - deficient mutant (V3177) were grown in iron replete conditions was used to compare to Porphyromonas gingivalis strains grown in iron chelated conditions.

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Porphyromonas gingivalis

Project description:Porphyromonas gingivalis Genome sequencing

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Role of RNA-binding protein, Pgr, in Porphyromonas gingivalis

Project description:Role of RNA-binding protein, Pgr, in Porphyromonas gingivalis.

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Treponema denticola gene expression during co-culture with Porphyromonas gingivalis

Project description:Porphyromonas gingivalis and Treponema denticola are periodontalpathogens that are associated with the severity and progression of periodontal diseases. this study investigates the gene expression of Treponema denticola during co-culture with Porphyromonas gingivalis.

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