Related Experiment Video
Updated: May 9, 2026

12:16
Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells
Published on: December 17, 2015
Macrophage subset sensitivity to endotoxin tolerisation by Porphyromonas gingivalis
1School of Biomedical and Biological Sciences, University of Plymouth, Plymouth, United Kingdom. andrew.foey@plymouth.ac.uk
Plos One
|July 23, 2013
Summary
Porphyromonas gingivalis selectively suppresses regulatory M2 macrophages, promoting oral inflammation. Pro-inflammatory M1 macrophages remain unaffected, potentially driving immunopathology in periodontal disease.
Area of Science:
- Immunology
- Oral Microbiology
- Cell Biology
Background:
- Macrophages (MΦs) are key in oral mucosal immunity, balancing tolerance and pathogen defense.
- Distinct M1 (pro-inflammatory) and M2 (regulatory) macrophage subsets mediate different immune responses.
- Chronic stimulation, like by LPS, can induce macrophage tolerance.
Purpose of the Study:
- To investigate how Porphyromonas gingivalis (PG) affects the susceptibility of M1 and M2 macrophage subsets to suppression.
- To determine if PG differentially impacts MΦ subsets involved in oral mucosal immunity.
Main Methods:
- In vitro generation of CD14(hi) and CD14(lo) M1 and M2 MΦs from THP-1 monocytes.
- Pre-treatment of MΦ subsets with heat-killed PG (HKPG) and PG-LPS.
- Stimulation with bacterial pathogen-associated molecular patterns (PAMPs) and measurement of inflammatory cytokines (TNFα, IL-1β, IL-6, IL-10) and NFκB activation.
Main Results:
- HKPG and PG-LPS differentially suppressed PAMP-induced TNFα, IL-6, and IL-10, but not IL-1β.
- P. gingivalis suppressed NFκB activation in M2 MΦs and CD14(lo) M1 MΦs.
- CD14(hi) M1 pro-inflammatory MΦs were resistant to P. gingivalis-mediated suppression.
Conclusions:
- P. gingivalis selectively induces tolerance in regulatory M2 macrophages.
- Pro-inflammatory CD14(hi) M1 macrophages are largely unaffected by P. gingivalis.
- This differential suppression may facilitate oral immunopathology at the expense of effective immunity.

