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Oral Microbiota and Immune System Crosstalk: A Translational Research
Andrea Ballini1,2,3, Gianna Dipalma4, Ciro Gargiulo Isacco3,4
1Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari "Aldo Moro", Campus Universitario "Ernesto Quagliariello", 70125 Bari, Italy.
Background:
Oral pathogens may exert the ability to trigger differently the activation of local macrophage immune responses, for instance Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans induce predominantly pro-inflammatory (M1-like phenotypes) responses, while oral commensal microbiota primarily elicits macrophage functions consistent with the anti-inflammatory (M2-like phenotypes).
Methods:
In healthy individuals vs. periodontal disease patients' blood samples, the differentiation process from monocyte to M1 and M2 was conducted using two typical growth factors, the granulocyte/macrophage colony stimulating factor (GM-CSF) and the macrophage colony stimulating factor (M-CSF).
Results:
In contrast with the current literature our outcomes showed a noticeable increase of macrophage polarization from healthy individuals vs. periodontal patients. The biological and clinical significance of these data was discussed.
Conclusions:
Our translational findings showed a significant variance between control versus periodontal disease groups in M1 and M2 marker expression within the second group significantly lower skews differentiation of M2-like macrophages towards an M1-like phenotype. Macrophage polarization in periodontal tissue may be responsible for the development and progression of inflammation-induced periodontal tissue damage, including alveolar bone loss, and modulating macrophage function may be a potential strategy for periodontal disease management.
Insights
Periodontal disease alters macrophage polarization, skewing M2-like macrophages towards an M1-like phenotype. Modulating macrophage function may offer a new strategy for managing periodontal disease and its associated tissue damage.
Area of Science:
- Immunology
- Oral Biology
- Periodontology
Background:
- Oral pathogens and commensals differentially activate macrophage immune responses.
- Pathogens like Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans promote pro-inflammatory (M1) phenotypes.
- Commensal microbiota typically induce anti-inflammatory (M2) macrophage phenotypes.
Purpose of the Study:
- To investigate macrophage polarization differences between healthy individuals and periodontal disease patients.
- To analyze the expression of M1 and M2 markers in monocytes from different patient groups.
Main Methods:
- Monocyte differentiation into M1 and M2 macrophages was induced using granulocyte/macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF).
- Blood samples from healthy individuals and periodontal disease patients were analyzed.
Main Results:
- Macrophage polarization showed a noticeable increase in healthy individuals compared to periodontal disease patients.
- A significant variance in M1 and M2 marker expression was observed between the groups.
- Periodontal disease patients exhibited a lower skewing of M2-like macrophages towards an M1-like phenotype.
Conclusions:
- Macrophage polarization plays a role in the development and progression of periodontal tissue damage, including alveolar bone loss.
- Findings suggest that altered macrophage polarization contributes to inflammation-induced damage in periodontal disease.
- Modulating macrophage function presents a potential therapeutic strategy for periodontal disease management.
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