Saliva initiates the formation of pro-inflammatory macrophages in vitro |
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| Institution: | 1. Department of Oral Biology, Dental School, Medical University of Vienna, Austria;2. Department of Preventive, Restorative and Pediatric Dentistry, School of Dental Medicine, University of Bern, Switzerland;3. Austrian Cluster for Tissue Regeneration, Austria;1. Department of Molecular and Developmental Medicine, University of Siena Viale Bracci, Siena, Italy;2. Department of Biotechnology, University of Siena, via Fiorentina 1, 53100 Siena, Italy;3. The University of Western Australia M460A, 35 Stirling Highway, Crawley, WA 6009, Australia;1. Department of Biological Physics, Eötvös Loránd University, Pázmány P. stny. 1/A, H-1117 Budapest, Hungary;2. Nanobiosensorics Group, Hungarian Academy of Sciences, Research Centre for Natural Sciences, Institute for Technical Physics and Materials Science, Konkoly-Thege út 29-33, H-1120 Budapest, Hungary;3. Doctoral School of Molecular- and Nanotechnologies, University of Pannonia, Veszprém, Hungary;4. MTA-ELTE Immunology Research Group, ELTE, Pázmány P. stny. 1/C, H-1117 Budapest, Hungary;5. Department of Immunology, Eötvös Loránd University, Pázmány P. stny. 1/C, H-1117 Budapest, Hungary;1. Servei de Pneumologia, Hospital Universitari Vall d’Hebron, Barcelona, España;2. Ciber de Enfermedades Respiratorias (CIBERES), Barcelona, España;1. Service de pédiatrie médicale, CHU de Caen, avenue Côte-de-Nacre, 14033 Caen, France;2. Laboratoire de virologie, CHU de Caen, avenue Clemenceau, 14033 Caen, France;3. Groupe de recherche sur l’adaptation microbienne (GRAM2), Normandie université, UNICAEN, UNIROUEN, 14000 Caen, France;1. Department of Conservative Dentistry and Periodontology, Medical University of Vienna, Austria;2. Austrian Cluster for Tissue Regeneration, Austria;3. Department of Oral Surgery, Medical University of Vienna, Austria;4. Laboratory of Oral Cell Biology, School of Dental Medicine, University of Bern, Switzerland |
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| Abstract: | ObjectivesSaliva can support oral wound healing, a process that requires a temporary inflammatory reaction. We have reported previously that saliva provokes a strong inflammatory response in oral fibroblasts. Bone marrow cells also give rise to macrophages, a heterogeneous subset of cell population involved in wound healing. Lipopolysaccharide (LPS) and interleukin 4 (IL-4) induce activation of pro-(M1), and anti-(M2) inflammatory macrophages, respectively. Yet, the impact of saliva on programming bone marrow cells into either M1 or M2 macrophages remains unclear .DesignHerein, we examined whether sterile saliva affects the in vitro process of macrophage polarization based on murine bone marrow cultures and RAW264.7 mouse macrophages.ResultsWe report that sterile saliva, similar to lipopolysaccharides, provoked a robust activation of the M1 phenotype which is characterized by a strong increase of the respective genes IL-12 and IL-6, based on a real-time gene expression analysis, and for IL-6 with immunoassay. Arginase-1 and Ym1, both genes characteristic for the M2 phenotype, were not considerably modulated by saliva. Inhibition of TLR4 signaling with TAK-242, blocking NFκB signaling with Bay 11-7085, but also autoclaving saliva greatly reduced the development of the M1 phenotype.ConclusionThese data suggest that saliva activates the TLR4 dependent polarization into pro-inflammatory M1 macrophages in vitro. |
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| Keywords: | Saliva Inflammation Primary macrophages RAW264 7 Mouse TLR4 |
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