J. Katz
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
J. Katz has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- C.L. Prairie
Department of Pediatric Dentistry, School of Dentistry, University of Alabama at Birmingham, Birmingham, AL, USA
1 shared publication - Kristina N. Valladares
Department of Pediatric Dentistry, School of Dentistry, University of Alabama at Birmingham, Birmingham, AL, USA
1 shared publication - Muhammad Shahid Riaz Rajoka
Laboratory of Animal Food Function, Graduate School of Agricultural Science, Tohoku University, Sendai 980-8572, Japan
1 shared publication - Peter H. King
Department of Neurology, University of Alabama at Birmingham, Birmingham, USA
1 shared publication - Ping Zhang
Department of Pediatric Dentistry, School of Dentistry, University of Alabama at Birmingham, Birmingham, AL, USA
1 shared publication - Suzanne M. Michalek
Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
1 shared publication
Latest Publications
- 24 September 2026
- Published by SAGE Publications in Journal of Dental Research
Porphyromonas gingivalis Promotes Lipid Droplet–Mediated Microglial Dysfunction
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 accumulation of lipid droplets (LD), 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 infection with Pg (ATCC 33277) induces robust LD accumulation in BV2 microglial cells and in microglia from Pg -infected App knock-in mice. This Pg -driven LD buildup was closely associated with elevated reactive oxygen species (ROS) production, impaired phagocytic ability, and altered activation. Notably, pharmacologic inhibition of LD with a long-chain fatty acyl-CoA synthetase 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 and inflammatory mediators 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.
- 24 September 2026
- Published by SAGE Publications in Journal of Dental Research
Porphyromonas gingivalis Promotes Lipid Droplet–Mediated Microglial Dysfunction
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 accumulation of lipid droplets (LD), 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 infection with Pg (ATCC 33277) induces robust LD accumulation in BV2 microglial cells and in microglia from Pg -infected App knock-in mice. This Pg -driven LD buildup was closely associated with elevated reactive oxygen species (ROS) production, impaired phagocytic ability, and altered activation. Notably, pharmacologic inhibition of LD with a long-chain fatty acyl-CoA synthetase 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 and inflammatory mediators 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.