Andrea Ballini1,2,3, Gianna Dipalma4, Ciro Gargiulo Isacco3,4, Mariarosaria Boccellino2, Marina Di Domenico2, Luigi Santacroce5, Kieu C D Nguyễn6, Salvatore Scacco3, Maura Calvani7, Anna Boddi8, Fabiana Corcioli8, Lucio Quagliuolo2, Stefania Cantore4, Francesco Saverio Martelli4,8,9, Francesco Inchingolo4. 1. Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari "Aldo Moro", Campus Universitario "Ernesto Quagliariello", 70125 Bari, Italy. 2. Department of Precision Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. 3. Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari "Aldo Moro", 70121 Bari, Italy. 4. Department of Interdisciplinary Medicine, University of Bari "Aldo Moro", 70121 Bari, Italy. 5. Ionian Department, Microbiology and Virology Laboratory, Policlinico University Hospital, University of Bari "Aldo Moro", 70124 Bari, Italy. 6. Human Stem Cell's HSC, Ho Chi Minh City 70000, Vietnam. 7. Division of Pediatric Oncology/Hematology, Meyer University Children's Hospital, 50139 Florence, Italy. 8. Biomolecular Diagnostic Srl, 50139 Florence, Italy. 9. IMI (International Microdentistry Institute), 50139 Florence, Italy.
Abstract
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.
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 diseasepatients' 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.
Authors: Luigi Santacroce; Michele Di Cosola; Lucrezia Bottalico; Skender Topi; Ioannis Alexandros Charitos; Andrea Ballini; Francesco Inchingolo; Angela Pia Cazzolla; Gianna Dipalma Journal: Viruses Date: 2021-03-26 Impact factor: 5.048
Authors: Nicole B Arweiler; Vivien Rahmel; Bilal Alashkar Alhamwe; Fahd Alhamdan; Michael Zemlin; Sébastien Boutin; Alexander Dalpke; Harald Renz Journal: Microorganisms Date: 2021-06-18