The Effect of Porphyromonas gingivalis Lipopolysaccharide-Induced Periodontitis in Rats Fed a High-Cholesterol Diet on Macrophage Number
Abstract
Introduction: Periodontitis is a chronic inflammatory condition of the tooth-supporting tissue. P. gingivalis, which produces virulence factors, including lipopolysaccharide (LPS), is the main pathogenic driver of periodontitis. However, the interaction between the innate immune system and periodontal pathogens in hyperlipidemia remains unclear. Objective: The aim of this study was to investigate the effect of a high-cholesterol diet (HCD) on macrophage activity in P. gingivalis LPS-induced periodontitis. Methods: Twenty-eight male Sprague Dawley rats were divided into four groups (n=7 rats each group): LPS-HCD, saline-HCD, LPS-basal diet (LPS-BD), and saline-BD. HCD group had been being feeding by high cholesterol diet (1% cholesterol (w/w) and 0.5% cholic acid (w/w)) for 30 days before were injected with 0.2 ml of P. gingivalis ATCC 3277 LPS (LPS-HCD group) and saline (saline-HCD group). The other two groups had been being feeding by normal basal diet for 30 days before were injected with 0.2 ml of P. gingivalis ATCC 3277 LPS (LPS-BD group) and saline (saline-BD group). Rats were sacrificed and lower jaws were harvested and embedded in paraffin. Paraffin section of lower right and left incisor were deparaffinized, rehydrated, and stained with hematoxylin & eosin (H&E). The total number of macrophages was counted using a light microscope at a magnification of 400× from 10 fields of view. Results: The number of macrophages in the LPS-HCD group was the highest compare to LPS- BD, saline-HCD, and saline-BD groups. In addition, LPS-BD group had higher number of macrophage than saline-BD group which had the lowest number of macrophages. Conclusion: HCD and P. gingivalis LPS-induced periodontitis can contribute to increasing of macrophage activity in periodontitis. Thus, HCD itself can enhance the process of inflammation in periodontitis.
References
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Suh JS, Kim S, Boström KI, Wang CY, Kim RH, Park NH. Periodontitis-induced systemic inflammation exacerbates atherosclerosis partly via endothelial–mesenchymal transition in mice. Int J Oral Sci. 2019;11(3).
Duque GA, Descoteaux A. Macrophage cytokines: involvement in immunity and infectious diseases. Front Immunol. 2014;5:491.
Ren J, Ding Y, Yu H, Zhou Y, Yu W. Effects on the expression of pro-inflammatory cytokines in the liver and spleen after oral administration of Porphyromonas gingivalis in mice. Biomed Res. 2018;29(8):1603–9.
Abraham S, Premnath A, Arunima PR, Kassim RM. Critical Appraisal of Bidirectional Relationship between Periodontitis and Hyperlipidemia. J Int Soc Prev Community Dent. 2019;9(2):112-8.
Duan Y, Zeng L, Zheng C, Song B, Li F, Kong X, et al. Inflammatory links between high fat diets and diseases. Front Immunol. 2018;9:1–10.
Thapa S, Wei F. Association between high serum total cholesterol and periodontitis: National Health and Nutrition Examination Survey 2011 to 2012 study of American adults. J Periodontol. 2016;87:1286‑94.
Mauricio D, Castelblanco E, Alonso N. Cholesterol and Inflammation in Atherosclerosis: An Immune-Metabolic Hypothesis. Nutrients. 2020;12(8):2444
Fu Y, Li X, Xu H, Gong Y, Yang Y. Effects of periodontal therapy on serum lipid profile and proinflammatory cytokines in patients with hyperlipidemia: A randomized controlled trial. Clin Oral Investig. 2016;20:1263‑9.
Fajardo M, Rocha M, Sánchez‑Marin F, Espinosa‑Chávez E. Effect of atorvastatin on chronic periodontitis: A randomized pilot study. J Clin Periodontol. 2010;37:1016‑22.
Lei L, Li H, Yan F, Xiao Y. Hyperlipidemia Impaired Innate Immune Response to Periodontal Pathogen Porphyromonas gingivalis in Apolipoprotein E Knockout Mice. PLoS One. 2013;8(8):1–14.
Ermawati T, Gandini Abdi Nagari DFI, Praharani D, Sari DS. Effect of lipopolysaccharide induction of Porphyromonas gingivalis on osteoclast and osteoblast cell number of wistar rats’ (Rattus norvegicus) alveolar bone. Int J Appl Pharm. 2019;11:64–7.
Fujita M, Numabe Y. Histological effects and pharmacokinetics of lipopolysaccharide derived from Porphyromonas gingivalis on rat maxilla and liver concerning with progression into non-alcoholic steatohepatitis. J Periodontol. 2018;89:1101–11.
Swanson L, Katkar GD, Tam J, Pranadinata RF, Chareddy Y, Coates J, et al. TLR4 signaling and macrophage inflammatory responses are dampened by GIV/Girdin. Proc Natl Acad Sci USA. 2020;117(43):26895–906.
Tomofuji T, Azuma T, Kusano H, Sanbe T, Ekuni D, Tamaki N, et al. Oxidative damage of periodontal tissue in the rat periodontitis model : Effects of a high-cholesterol diet. Fed Eur Biochem Soc (FEBS) Lett. 2006;580:3601–4.
Varela-López A, Bullón P, Ramírez-Tortosa CL, Navarro-Hortal MD, Robles-Almazán M, Bullón B, et al. A diet rich in saturated fat and cholesterol aggravates the effect of bacterial lipopolysaccharide on alveolar bone loss in a rabbit model of periodontal disease. Nutrients. 2020;12(5):1405
Published
2021-10-31
How to Cite
SARI, Finsa Tisna et al.
The Effect of Porphyromonas gingivalis Lipopolysaccharide-Induced Periodontitis in Rats Fed a High-Cholesterol Diet on Macrophage Number.
Journal of Indonesian Dental Association, [S.l.], v. 4, n. 2, p. 117-121, oct. 2021.
ISSN 2621-6175.
Available at: <http://jurnal.pdgi.or.id/index.php/jida/article/view/637>. Date accessed: 21 nov. 2024.
doi: https://doi.org/10.32793/jida.v4i2.637.
Section
Research Article
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.