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Updated: May 19, 2026
Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells
Published on: December 17, 2015
Porphyromonas gingivalis promotes lipid droplet-mediated microglial dysfunction
Muhammad Shahid Riaz Rajoka1, Kristina Nicole Valladares1, Chloe La Prairie1
1Department of Pediatric Dentistry, School of Dentistry, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Abstract:
Growing evidence supports a strong association between periodontitis and Alzheimer's disease (AD), yet the mechanisms linking these conditions remain poorly defined. In neurodegenerative disorders, including AD, microglia are often characterized by increased lipid droplet (LD) accumulation, heightened activation, and impaired function. In this study, we examined whether Porphyromonas gingivalis (Pg), a keystone periodontal pathogen, promotes LD accumulation in microglia and disrupts their function. We found that Pg infection induces robust LD accumulation in BV2 microglial cells and in microglia from Pg-infected App KI mice. This Pg-driven LD buildup was closely associated with elevated reactive oxygen species (ROS) production, impaired phagocytic ability, and altered activation. Notably, pharmacological inhibition of LD with a triglyceride synthesis inhibitor effectively reversed Pg-induced LD accumulation, mitigated ROS production, and restored phagocytic function, thus underscoring the critical role of lipid metabolism in regulating microglial function. These findings support a model in which, in the context of periodontitis, systemic dissemination of periodontal pathogens promotes LD accumulation in microglia, and this metabolic alteration exacerbates microglia dysfunction via a self-reinforcing cycle of excessive oxidative stress and impaired phagocytosis, potentially accelerating AD progression.
Insights
Periodontitis-causing bacteria, Porphyromonas gingivalis, trigger lipid droplet buildup in microglia. This impairs their function and may accelerate Alzheimer's disease progression.
Area of Science:
- Neuroimmunology
- Microbial Pathogenesis
- Neurodegenerative Diseases
Background:
- Periodontitis and Alzheimer's disease (AD) share a strong association, but underlying mechanisms are unclear.
- Microglia, the brain's immune cells, show lipid droplet accumulation and dysfunction in neurodegenerative disorders like AD.
- Porphyromonas gingivalis (Pg) is a key pathogen in periodontitis.
Purpose of the Study:
- To investigate if Porphyromonas gingivalis (Pg) induces lipid droplet (LD) accumulation in microglia.
- To determine the impact of Pg-induced LD accumulation on microglial function.
- To explore the role of lipid metabolism in microglial dysfunction during periodontitis.
Main Methods:
- Infection of BV2 microglial cells and microglia from Pg-infected App KI mice with Porphyromonas gingivalis.
- Assessment of lipid droplet accumulation, reactive oxygen species (ROS) production, and phagocytic ability.
- Pharmacological inhibition of lipid droplet synthesis using a triglyceride synthesis inhibitor.
Main Results:
- Pg infection robustly increased LD accumulation in microglia.
- Pg-induced LD buildup correlated with increased ROS production, impaired phagocytosis, and altered microglial activation.
- Inhibiting LD synthesis reversed these functional deficits, highlighting lipid metabolism's role.
Conclusions:
- Porphyromonas gingivalis promotes lipid droplet accumulation in microglia, contributing to their dysfunction.
- This microglial metabolic alteration exacerbates oxidative stress and impairs phagocytosis, potentially accelerating Alzheimer's disease progression.
- Targeting lipid metabolism may offer a therapeutic strategy for periodontitis-associated neuroinflammation.
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