Effect of Bacterial Infection on Ghrelin Receptor Regulation in Periodontal Cells and Tissues

• Published in: International journal of molecular sciences 2022-03, Vol.23 (6), p.3039
• Main Authors: Nogueira, Andressa V B, Nokhbehsaim, Marjan, Damanaki, Anna, Eick, Sigrun, Beisel-Memmert, Svenja, Kirschneck, Christian, Schröder, Agnes, Cirelli, Thamiris, Leguizamón, Natalia D P, Cirelli, Joni A, Deschner, James
• Format: Article
• Language: English
• Subjects: Animals; Bacteria; Bacterial infections; Bacterial Infections - metabolism; Cell viability; Cytokines; Evaluation; Fusobacterium nucleatum; Gene expression; Ghrelin; Ghrelin - metabolism; Ghrelin - pharmacology; ghrelin receptor; Gingiva - metabolism; Gum disease; human gingival fibroblast; Hypothalamus; Immunocytochemistry; Inflammation; Interleukin 6; Monocyte chemoattractant protein 1; periodontal tissues; Periodontitis; Periodontitis - metabolism; Proteins; Rats; Receptors, Ghrelin - genetics; Receptors, Ghrelin - metabolism; Systemic diseases; Tumor necrosis factor-TNF; Wound healing
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms23063039

The effect of bacterial infection on the expression of growth hormone secretagogue receptor (GHS-R) was investigated in periodontal cells and tissues, and the actions of ghrelin were evaluated. GHS-R was assessed in periodontal tissues of rats with and without periodontitis. Human gingival fibroblasts (HGFs) were exposed to in the presence and absence of ghrelin. GHS-R expression was determined by real-time PCR and immunocytochemistry. Furthermore, wound healing, cell viability, proliferation, and migration were evaluated. GHS-R expression was significantly higher at periodontitis sites as compared to healthy sites in rat tissues. significantly increased the GHS-R expression and protein level in HGFs. Moreover, ghrelin significantly abrogated the stimulatory effects of on CCL2 and IL-6 expressions in HGFs and did not affect cell viability and proliferation significantly. Ghrelin stimulated while decreased wound closure, probably due to reduced cell migration. Our results show original evidence that bacterial infection upregulates GHS-R in rat periodontal tissues and HGFs. Moreover, our study shows that ghrelin inhibited the proinflammatory actions of on HGFs without interfering with cell viability and proliferation, suggesting that ghrelin and its receptor may act as a protective molecule during bacterial infection on periodontal cells.