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Open AccessArticle

Oral Microbiota and Immune System Crosstalk: A Translational Research

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Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari “Aldo Moro”, Campus Universitario “Ernesto Quagliariello”, 70125 Bari, Italy
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Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, 80138 Naples, Italy
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Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari “Aldo Moro”, 70121 Bari, Italy
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Department of Interdisciplinary Medicine, University of Bari “Aldo Moro”, 70121 Bari, Italy
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Ionian Department, Microbiology and Virology Laboratory, Policlinico University Hospital, University of Bari “Aldo Moro”, 70124 Bari, Italy
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Human Stem Cell’s HSC, Ho Chi Minh City 70000, Vietnam
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Division of Pediatric Oncology/Hematology, Meyer University Children’s Hospital, 50139 Florence, Italy
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Biomolecular Diagnostic Srl, 50139 Florence, Italy
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IMI (International Microdentistry Institute), 50139 Florence, Italy
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work as co-first Authors.
These authors contributed equally to this work as co-last Authors.
Biology 2020, 9(6), 131; https://doi.org/10.3390/biology9060131
Received: 7 May 2020 / Revised: 10 June 2020 / Accepted: 12 June 2020 / Published: 16 June 2020
(This article belongs to the Special Issue Microbiota and Immune System Crosstalk 2020)
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. View Full-Text
Keywords: microbiota; periodontal disease; immune system; lymphocytes; macrophage polarization; oral pathology; oral-systemic disease; clinical microbiology; clinical biochemistry; translational research microbiota; periodontal disease; immune system; lymphocytes; macrophage polarization; oral pathology; oral-systemic disease; clinical microbiology; clinical biochemistry; translational research
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Ballini, A.; Dipalma, G.; Isacco, C.G.; Boccellino, M.; Di Domenico, M.; Santacroce, L.; Nguyễn, K.C.; Scacco, S.; Calvani, M.; Boddi, A.; Corcioli, F.; Quagliuolo, L.; Cantore, S.; Martelli, F.S.; Inchingolo, F. Oral Microbiota and Immune System Crosstalk: A Translational Research. Biology 2020, 9, 131.

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