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ORIGINAL RESEARCH article

Front. Cell Dev. Biol.
Sec. Cell Death and Survival
Volume 13 - 2025 | doi: 10.3389/fcell.2025.1419651

Porphyromonas gingivalis affects neutrophil pro-inflammatory activities

Provisionally accepted
Agnieszka Zimny Agnieszka Zimny 1Alicja Płonczyńska Alicja Płonczyńska 1Wiktor Jakubowski Wiktor Jakubowski 1Natalia Zubrzycka Natalia Zubrzycka 1Jan Potempa Jan Potempa 1,2Maja Sochalska Maja Sochalska 1*
  • 1 Department of Microbiology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Kraków, Lesser Poland, Poland
  • 2 School of Dentistry, University of Louisville, Louisville, Colorado, United States

The final, formatted version of the article will be published soon.

    Porphyromonas gingivalis is the primary pathogen responsible for the development of periodontal inflammatory disease. Although gingipains are the major virulence factor of the pathogen, their role in impairing apoptosis and immune cell function is not fully understood.To investigate the impact of gingipains on neutrophil viability and function, we conducted studies using murine HoxB8 neutrophils and primary human neutrophils infected with wildtype strains of P. gingivalis (W83 and ATCC 33277), or a gingipains-null mutant with deleted gingipains encoding genes, or wild-type bacteria preincubated with specific gingipain inhibitors. Flow cytometry revealed that wild-type P. gingivalis had a marked effect on neutrophil viability regulated by anti-apoptotic proteins belonging to the Bcl-2 family; however, these effects were independent of gingipain expression or activity. Importantly, experiments using primary human neutrophils and macrophages revealed that gingipains play a significant role in the disruption of immune cell functions via the induction of reactive oxygen species and inactivation of neutrophil elastase activity. Additionally, although gingipains

    Keywords: Porphyromonas gingivalis, Gingipains, Bcl-2 family proteins, Apoptosis, Neutrophils, Macrophages, periodontitis (Min. 5-Max. 8)

    Received: 18 Apr 2024; Accepted: 13 Jan 2025.

    Copyright: © 2025 Zimny, Płonczyńska, Jakubowski, Zubrzycka, Potempa and Sochalska. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Maja Sochalska, Department of Microbiology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Kraków, 30-387, Lesser Poland, Poland

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