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Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells

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Published on: December 17, 2015

ATF5-mediated mitochondrial UPR inhibited RANKL in Porphyromonas gingivalis LPS-treated osteoblasts.

Tianrui Yang¹, Weiman Sun², Lang Lei²

¹Shanghai Jiading District Central Hospital, Shanghai, China; Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.

Archives of Oral Biology

|February 27, 2026

Summary

The mitochondrial unfolded protein response (UPR^mt) is induced by Porphyromonas gingivalis-lipopolysaccharide (P. gingivalis-LPS) and regulates bone resorption in periodontitis. Enhancing UPR^mt may offer a therapeutic target for periodontitis.

Keywords:

Activating transcription factor 5 Mitochondrial unfolded protein response Porphyromonas gingivalis Reactive oxygen species

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Area of Science:

Molecular Biology
Cell Biology
Periodontology

Background:

Periodontitis involves bone resorption, potentially linked to mitochondrial dysfunction.
The mitochondrial unfolded protein response (UPR^mt) is a cellular stress response.
Porphyromonas gingivalis lipopolysaccharide (P. gingivalis-LPS) is a key pathogen in periodontitis.

Purpose of the Study:

Investigate UPR^mt induction in P. gingivalis-LPS-treated osteoblasts.
Examine the relationship between UPR^mt, mitochondrial function, and bone resorption.
Determine the role of ATF5 in UPR^mt-mediated regulation of bone metabolism.

Main Methods:

Osteoblasts were treated with P. gingivalis-LPS.
UPR^mt was modulated using nicotinamide riboside (NR), doxycycline (DOX), or ATF5 knockdown.
Gene and protein expression, mitochondrial function (ROS, membrane potential), and RANKL/OPG levels were assessed.

Main Results:

P. gingivalis-LPS induced UPR^mt and RANKL expression in osteoblasts.
Enhanced UPR^mt reduced RANKL and the RANKL/osteoprotegerin (OPG) ratio.
ATF5 knockdown worsened mitochondrial dysfunction and increased RANKL expression.

Conclusions:

ATF5-mediated UPR^mt regulates RANKL expression via mitochondrial reactive oxygen species (mtROS) and mitochondrial membrane potential.
UPR^mt is a potential therapeutic target for managing bone resorption in periodontitis.