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Published on: December 20, 2018
Bacterial sialoglycosidases in Virulence and Pathogenesis
Preethi Sudhakara1, Iyappan Sellamuthu2, A Wilson Aruni3,4,5
1Department of Genetic Engineering, SRM Institute of Science and Technology, Chennai 603203, India. miyupreethi@gmail.com.
Human oral microbiome dysbiosis, often caused by immune impairment, can lead to periodontitis. Porphyromonas gingivalis uses sialoglycoproteases to disrupt host defenses, offering potential drug targets.
Area of Science:
- Microbiology
- Immunology
- Periodontology
Background:
- Human oral microbiome dysbiosis is linked to immune system impairment and chronic inflammatory diseases like periodontitis.
- Periodontitis affects millions, increasing risks for systemic conditions including cardiovascular disease and Alzheimer's disease.
- Porphyromonas gingivalis is a keystone pathogen driving periodontitis by subverting host defenses and altering the oral microbiota.
Purpose of the Study:
- To investigate the role of Porphyromonas gingivalis sialoglycoproteases in oral dysbiosis.
- To understand microbial strategies targeting host sialoglycoproteins for immune dysregulation.
- To identify potential therapeutic targets for periodontitis and related conditions.
Main Methods:
- Analysis of Porphyromonas gingivalis virulence factors.
- Investigation of microbial enzyme activity on host sialoglycoproteins.
- Exploration of sialic acid-mediated pathogen-toll like receptor (TLR) interactions.
Main Results:
- Porphyromonas gingivalis employs sialoglycoproteases to degrade host sialoglycoproteins, exposing terminal sialic acid.
- This process facilitates immune dysregulation and pathogen growth.
- Sialic acid-mediated interactions with pathogen toll-like receptors (TLRs) are implicated in dysbiosis.
Conclusions:
- Porphyromonas gingivalis sialoglycoproteases are key virulence factors in periodontitis.
- Understanding these enzymes' function is crucial for developing novel therapeutic strategies.
- Carbohydrate analogues and sialic acid mimetics show promise as drug targets against P. gingivalis-mediated dysbiosis.
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