dc.contributor.author | Hastürk, Hatice | |
dc.contributor.author | Kantarcı, Alpdoğan | |
dc.contributor.author | Stephans, D | |
dc.contributor.author | Fıratlı, Halil Erhan | |
dc.contributor.author | Vandyke, Thomas | |
dc.contributor.author | Öner, Fatma | |
dc.contributor.author | Yaghmoor, Wael | |
dc.date.accessioned | 2022-07-04T12:27:08Z | |
dc.date.available | 2022-07-04T12:27:08Z | |
dc.identifier.citation | Öner F., Yaghmoor W., Stephans D., Hastürk H., Fıratlı H. E. , Vandyke T., Kantarcı A., "Resolving E1 regulates inflammatory cellinfiltration and cytokine production in diabeticperiodontitis", EuroPerio 10, Kobenhavn, Danimarka, 15 - 18 Haziran 2022, cilt.49, sa.6, ss.6 | |
dc.identifier.other | vv_1032021 | |
dc.identifier.other | av_1d0694ae-ee2c-4d1a-980e-05cb16cd671b | |
dc.identifier.uri | http://hdl.handle.net/20.500.12627/181847 | |
dc.identifier.uri | https://onlinelibrary.wiley.com/toc/1600051x/2022/49/S23 | |
dc.identifier.uri | https://doi.org/10.1111/jcpe.13634 | |
dc.description.abstract | Background and Aim: Diabetic periodontitis involves a complexinflammatory process where periodontitis and diabetes aggravate theseverity of the other. We hypothesized that Resolvin E1 (RvE1), apro-resolution mediator of inflammation, decreases inflammatory cellinfiltrate and pro-inflammatory cytokine expression in diabeticperiodontitis through active ligand-receptor activation.Methods: The db/db mouse (leptin receptor mutation) was crossbredwith ERV1 transgenic mice (overexpresses receptor for RvE1) to gener-ate double-mutant mice (db/db-ERV1).Wild-type (WT) and transgenicmice overexpressing ERV1 only were used as controls. Experimentalperiodontitis was induced with 7-0 silk ligatures tied around the maxillarysecond molars. Half of the animals received 10 mM RvE1 daily for7 days. Gingival expression of IL-17+and IL-2+cells was evaluated byimmunohistochemistry. Peripheral blood serum samples were tested forIL-17A, IL-17F, CCL20, IL-6, and IL-10 by multiplex immunoassay.Results: Diabetic mice exhibited significantly more bone loss, withincreased levels of IL-6, IL-17, CCL20, and IL-10 at baseline comparedto the WT animals (p < 0.001). db/db-ERV1 mice were protected fromthe increased inflammatory phenotype and periodontal disease(p < 0.001 compared to db/db mice). Experimental periodontitis led toa significant increase in cytokine levels in all groups; however, it wassignificantly lower in the db/db-ERV1 mice compared to the diabeticand WT groups (p < 0.05). RvE1 treatment prevented experimentalperiodontitis-induced cytokine production in all groups; with a moresignificant impact on the db/db ERV1 group. Periodontitis increasedthe percentage of IL-17+cells in tissues in all groups; RvE1 treatmentprevented this increase in ERV1, db/db, and db/ERV1 mice anddecreased IL-2+cells in db/db and db/db ERV1 mice (p < 0.05).Conclusions: RvE1 resolves inflammation and restores periodontalhomeostasis through receptor-mediated activity and prevents excessinflammation induced by periodontitis in diabetic mice | |
dc.language.iso | eng | |
dc.subject | Orthodontics | |
dc.subject | Oral Surgery | |
dc.subject | Dentistry (miscellaneous) | |
dc.subject | Dental Hygiene | |
dc.subject | Periodontics | |
dc.subject | Dental Assisting | |
dc.subject | General Dentistry | |
dc.subject | Health Sciences | |
dc.subject | Klinik Bilimler | |
dc.subject | Periodontoloji | |
dc.subject | Diş Hekimliği | |
dc.subject | Sağlık Bilimleri | |
dc.subject | DİŞ HEKİMLİĞİ, ORAL CERRAHİ VE TIP | |
dc.subject | Klinik Tıp | |
dc.subject | Klinik Tıp (MED) | |
dc.title | Resolving E1 regulates inflammatory cellinfiltration and cytokine production in diabeticperiodontitis | |
dc.type | Bildiri | |
dc.contributor.department | Bahçeşehir Üniversitesi , Diş Hekimliği Fakültesi , Klinik Bilimler Bölümü | |
dc.identifier.volume | 49 | |
dc.contributor.firstauthorID | 3432592 | |