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Updated: Aug 7, 2026

Isolation, Processing and Analysis of Murine Gingival Cells
Published on: July 2, 2013
Molecular mediators of Porphyromonas gingivalis-induced T-cell apoptosis
J I Harris1, R R B Russell, M A Curtis
1Department of Oral Biology, The Dental School, University of Newcastle upon Tyne, Newcastle upon Tyne, UK.
Abstract:
Porphyromonas gingivalis produces virulence factors which can modify the molecular and cellular components of the host immune response. In the present work we investigated the role of specific virulence factors from P. gingivalis in the induction of apoptosis in Jurkat T cells. P. gingivalis culture supernatants mimicked the effect of butyric acid on T-cell apoptosis and this effect was associated with an increase in histone H4 acetylation. A role for proteases was excluded in experiments which demonstrated that neither protease inhibitors nor use of P. gingivalis mutants defective in protease synthesis had any effect on the stimulation of T-cell apoptosis in this system.
Insights
Porphyromonas gingivalis culture supernatants induce T-cell apoptosis by increasing histone H4 acetylation, independent of proteases. This finding sheds light on bacterial virulence mechanisms affecting immune cells.
Area of Science:
- Microbiology
- Immunology
- Molecular Biology
Background:
- Porphyromonas gingivalis is a bacterium known to produce virulence factors that influence host immune responses.
- Understanding how these virulence factors impact immune cells, such as T cells, is crucial for comprehending host-pathogen interactions.
Purpose of the Study:
- To investigate the role of specific P. gingivalis virulence factors in inducing apoptosis in Jurkat T cells.
- To elucidate the molecular mechanisms underlying T-cell apoptosis triggered by P. gingivalis.
Main Methods:
- Incubation of Jurkat T cells with P. gingivalis culture supernatants.
- Assessment of apoptosis induction.
- Analysis of histone H4 acetylation levels.
- Experiments using protease inhibitors and P. gingivalis protease-deficient mutants.
Main Results:
- P. gingivalis culture supernatants induced apoptosis in Jurkat T cells, similar to butyric acid.
- This apoptosis induction was correlated with increased histone H4 acetylation.
- Proteases from P. gingivalis were found not to be responsible for stimulating T-cell apoptosis.
Conclusions:
- P. gingivalis virulence factors, independent of proteases, can induce T-cell apoptosis.
- Histone H4 acetylation is implicated in the apoptotic process mediated by P. gingivalis supernatants.
- These findings contribute to understanding how oral bacteria modulate host immune cell function.
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