Abstract
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 Fusobacterium nucleatum 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. F. nucleatum significantly increased the GHS-R expression and protein level in HGFs. Moreover, ghrelin significantly abrogated the stimulatory effects of F. nucleatum on CCL2 and IL-6 expressions in HGFs and did not affect cell viability and proliferation significantly. Ghrelin stimulated while F. nucleatum 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 F. nucleatum 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.
Highlights
Licensee MDPI, Basel, Switzerland.Lately, periodontal disease has been considered as one of the most prevalent human pathologies worldwide [1]
Our findings suggest that ghrelin and its receptor may act as important protective molecules during bacterial infection on Human gingival fibroblasts (HGFs) by increasing growth hormone secretagogue receptor (GHS-R) and favoring wound healing through its anti-inflammatory and migration potential actions
Our study yields original evidence that GHS-R expression is enhanced by bacterial infection in rat periodontal tissues in vivo and in HGFs in vitro
Summary
Licensee MDPI, Basel, Switzerland.Lately, periodontal disease has been considered as one of the most prevalent human pathologies worldwide [1]. Periodontitis is a chronic inflammatory disease with a serious impact on different aspects of an individual’s life, leading to masticatory dysfunction and oral disability, impaired quality of life, social problems, and a significant economic burden [2–4]. It is a multifactorial disease characterized by the loss of tooth-supporting tissues such as gingiva, periodontal ligament, cementum, and alveolar bone, and it is published maps and institutional affil-. A complex interaction between periodontopathogens and host immunity arises so that host resident and infiltrating cells are activated These cells produce various proinflammatory mediators, including interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor (TNF)-α, cyclooxygenase-2 (COX2), and chemokine CC motif ligand 2 (CCL2), as well as matrix-degrading proteases such as matrix metalloproteinases [5–7]. If the host immune response is insufficient to remove the microbial challenge, it may cause chronic inflammation, which leads to irreversible degradation of the extracellular matrix and resorption of the alveolar bone, resulting in periodontal breakdown and even tooth loss
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