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IL-36γ is a pivotal inflammatory player in periodontitis-associated bone loss

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Title: IL-36γ is a pivotal inflammatory player in periodontitis-associated bone loss
Authors: Isaac Maximiliano Bugueno, Sophie Sourice, Olivier Huck, Valérie Geoffroy, Philippe Lesclous, Alexandra Cloitre, Jérôme Guicheux, Fareeha Batool, Boris Halgand, Jocelyne Caillon
Contributors: Jehan, Frederic, Regenerative Medicine and Skeleton (RMeS), École nationale vétérinaire, agroalimentaire et de l'alimentation Nantes-Atlantique (ONIRIS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Universitaire de Nantes = Nantes University Hospital (CHU Nantes)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Université de Nantes - UFR Odontologie (UFR Odonto), Université de Nantes (UN), Laboratoire d'ingénierie osteo-articulaire et dentaire (LIOAD), IFR26-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR Odontologie (UFR Odonto), Centre Hospitalier Universitaire de Nantes = Nantes University Hospital (CHU Nantes), Nanomédecine Régénérative (NanoRegMed), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)
Source: Sci Rep
Publisher Information: Springer Science and Business Media LLC, 2019.
Publication Year: 2019
Subject Terms: Male, 0301 basic medicine, MESH: Alveolar Bone Loss / microbiology, MESH: Alveolar Bone Loss / metabolism, Alveolar Bone Loss, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, Article, Cell Line, MESH: Inflammation / microbiology, 03 medical and health sciences, MESH: Bacteroidaceae Infections / metabolism, MESH: Inflammation / metabolism, Bacteroidaceae Infections, Humans, MESH: Interleukin-1 / metabolism, Periodontitis, [SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunity, MESH: Periodontitis / microbiology, MESH: Bacteroidaceae Infections / pathology, Inflammation, Molecular Biology/Genomics [q-bio.GN], 0303 health sciences, MESH: Humans, MESH: Inflammation / pathology, MESH: Male, MESH: Cell Line, 3. Good health, MESH: Alveolar Bone Loss / pathology, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], MESH: Periodontitis / metabolism, Female, MESH: Periodontitis / pathology, MESH: Porphyromonas gingivalis / metabolism, MESH: Female, Porphyromonas gingivalis, Interleukin-1
Description: Periodontitis is a prevalent chronic inflammatory disease due to the host response (IL-1β, IL-6, TNF-α and IL-17A) to oral bacteria such as Porphyromonas gingivalis. The newer members of the IL-1 family, IL-36s (IL-36α/IL-36β/IL-36γ/IL-36Ra/IL-38) are known to be involved in host defense against P. gingivalis in oral epithelial cells (OECs) and are considered as key inflammatory mediators in chronic diseases. The aim of this study was to investigate the potential role of IL-36s in periodontitis. We showed here that IL-36γ mRNA gingival expression is higher in periodontitis patients, whereas IL-36β and IL-36Ra mRNA expression are lower compared to healthy controls. Interestingly, the elevated IL-36γ expression in patients is positively correlated with the RANKL/OPG ratio, an index of bone resorption. In vitro, IL-36γ expression was induced through TLR2 activation in primary OECs infected with P. gingivalis but not in gingival fibroblasts, the most widespread cell type in gingival connective tissue. In OECs, recombinant IL-36γ enhanced the expression of inflammatory cytokines (IL-1β, IL-6, TNF-α and IL-36γ), of TLR2 and importantly, the RANKL/OPG ratio. These findings suggest that IL-36γ could be a pivotal inflammatory player in periodontitis by perpetuating gingival inflammation and its associated alveolar bone resorption and could be a relevant therapeutic target.
Document Type: Article
Conference object
Other literature type
File Description: application/pdf
Language: English
ISSN: 2045-2322
DOI: 10.1038/s41598-019-55595-9
Access URL: https://www.nature.com/articles/s41598-019-55595-9.pdf
https://pubmed.ncbi.nlm.nih.gov/31848404
https://europepmc.org/article/MED/31848404
https://ui.adsabs.harvard.edu/abs/2019NatSR...919257C/abstract
https://www.nature.com/articles/s41598-019-55595-9.pdf
https://hal.archives-ouvertes.fr/hal-02418941
https://hal.archives-ouvertes.fr/hal-02418941/document
https://pubmed.ncbi.nlm.nih.gov/31848404/
https://hal.science/hal-02418941v1/document
https://hal.science/hal-02418941v1
https://doi.org/10.1038/s41598-019-55595-9
Rights: CC BY
Accession Number: edsair.doi.dedup.....38aefec2bde152ed1f7286622fb96896
Database: OpenAIRE
Description
Abstract:Periodontitis is a prevalent chronic inflammatory disease due to the host response (IL-1β, IL-6, TNF-α and IL-17A) to oral bacteria such as Porphyromonas gingivalis. The newer members of the IL-1 family, IL-36s (IL-36α/IL-36β/IL-36γ/IL-36Ra/IL-38) are known to be involved in host defense against P. gingivalis in oral epithelial cells (OECs) and are considered as key inflammatory mediators in chronic diseases. The aim of this study was to investigate the potential role of IL-36s in periodontitis. We showed here that IL-36γ mRNA gingival expression is higher in periodontitis patients, whereas IL-36β and IL-36Ra mRNA expression are lower compared to healthy controls. Interestingly, the elevated IL-36γ expression in patients is positively correlated with the RANKL/OPG ratio, an index of bone resorption. In vitro, IL-36γ expression was induced through TLR2 activation in primary OECs infected with P. gingivalis but not in gingival fibroblasts, the most widespread cell type in gingival connective tissue. In OECs, recombinant IL-36γ enhanced the expression of inflammatory cytokines (IL-1β, IL-6, TNF-α and IL-36γ), of TLR2 and importantly, the RANKL/OPG ratio. These findings suggest that IL-36γ could be a pivotal inflammatory player in periodontitis by perpetuating gingival inflammation and its associated alveolar bone resorption and could be a relevant therapeutic target.
ISSN:20452322
DOI:10.1038/s41598-019-55595-9