Marketing deregulated expression of anti-apoptotic proteins belonging to the Bcl-2 family in neutrophils as a potential therapy against periodontal disease. In vitro and in vivo analysis. (Q84300): Difference between revisions
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Revision as of 05:23, 29 October 2020
Project Q84300 in Poland
| Language | Label | Description | Also known as |
|---|---|---|---|
| English | Marketing deregulated expression of anti-apoptotic proteins belonging to the Bcl-2 family in neutrophils as a potential therapy against periodontal disease. In vitro and in vivo analysis. |
Project Q84300 in Poland |
Statements
2,000,000.0 zloty
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2,000,000.0 zloty
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100.0 percent
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1 April 2019
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31 March 2022
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UNIWERSYTET JAGIELLOŃSKI
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Chronic periodontal disease(PD) is one of the most frequent inflammatory diseases affecting 11.2% of the world’s population and representing a prominent public health burden. Risk factors for developing PD are cigarette smoking, diabetes, osteoporosis, and infections with periodontal pathogens(i.e. Porphyromonas gingivalis). The pathogenesis of PD is associated with an over-reactive host inflammatory response to P.gingivalis. Current literature implicates hyper-reactive neutrophils as the main immune cell type responsible for the tissue damage and the disease progression. Neutrophils have very short lifespan, controlled by the Bcl-2 family proteins, but it can be significantly prolonged during the infection. Therefore, I hypothesize that hyper-activity and prolonged survival of neutrophils induced by P.gingivalis through the increased expression of pro-survival members of the Bcl-2 family proteins is a novel, yet uncharacterized mechanism strongly contributing to the development of PD. (Polish)
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Chronic periodontal disease(PD) is one of the most frequent inflammatory diseases affecting 11.2 % of the world’s population and representing a prominent public health burden. Risk factors for developing PD are cigarette smoking, diabetes, osteoporosis, and infections with periodontal Pathogens(i.e. Porphyromonas gingivalis). The pathogenesis of PD is associated with an over-reactive host inflammatory response to P.gingivalis. Current literature implicates hyper-reactive neutrophils as the main immune cell type responsible for the tissue damage and the disease progression. Neutrophils have very short LifeSpan, controlled by the Bcl-2 family proteins, but it can be significantly prolonged during the infection. Thus, I hypothesise that hyper-activity and prolonged survival of neutrophils induced by P.gingivalis through the increased expression of pro-survival members of the Bcl-2 family proteins is a novel, yet uncharacterised mechanism strongly contributing to the development of PD. (English)
14 October 2020
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Identifiers
POIR.04.04.00-00-42FE/17
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