LPS from Negatively Alters Gingival Cell Mitochondrial Bioenergetics

Overview

Journal Int J Dent

Publisher Wiley

Specialty Dentistry

Date 2017 Jun 9

PMID 28592970

Citations 9

Authors

Kiran Napa

Andrea C Baeder

Jeffrey E Witt

Sarah T Rayburn

Madison G Miller

Blake W Dallon

Jonathan L Gibbs

Shalene H Wilcox

Duane R Winden

Jared H Smith

Paul R Reynolds

Benjamin T Bikman

Affiliations

Soon will be listed here.

Abstract

Objective: Oral inflammatory pathologies are linked to increased oxidative stress, thereby partly explaining their relevance in the etiology of systemic disorders. The purpose of this work was to determine the degree to which LPS from , the primary pathogen related to oral inflammation, altered gingival mitochondrial function and reactive oxygen species generation.

Methods: Human gingival fibroblast (HGF-1) cells were treated with lipopolysaccharide of Mitochondrial function was determined via high-resolution respirometry.

P Gingivalis: Mitochondrial function was determined via high-resolution respirometry.

Results: LPS-treated HGF-1 cells had significantly higher mitochondrial complex IV and higher rates of mitochondrial respiration. However, this failed to translate into greater ATP production, as ATP production was paradoxically diminished with LPS treatment. Nevertheless, production of the reactive HO was elevated with LPS treatment.

Conclusions: LPS elicits an increase in gingival cell mitochondria content, with a subsequent increase in reactive oxygen species production (i.e., HO), despite a paradoxical reduction in ATP generation. These findings provide an insight into the nature of oxidative stress in oral inflammatory pathologies.

Citing Articles

Endurance exercise-induced histone methylation modification involved in skeletal muscle fiber type transition and mitochondrial biogenesis.

Li J, Zhang S, Li C, Zhang X, Shan Y, Zhang Z Sci Rep. 2024; 14(1):21154.

PMID: 39256490 PMC: 11387812. DOI: 10.1038/s41598-024-72088-6.

The multifaceted role of c-di-AMP signaling in the regulation of lipopolysaccharide structure and function.

Ghods S, Muszynski A, Yang H, Seelan R, Mohammadi A, Hilson J Front Cell Infect Microbiol. 2024; 14:1418651.

PMID: 38933693 PMC: 11199400. DOI: 10.3389/fcimb.2024.1418651.

Ceramides Mediate Insulin-Induced Impairments in Cerebral Mitochondrial Bioenergetics in ApoE4 Mice.

Carr S, Saito E, Walton C, Saito J, Hanegan C, Warren C Int J Mol Sci. 2023; 24(23).

PMID: 38068958 PMC: 10706658. DOI: 10.3390/ijms242316635.

Mitochondrial Dysfunction in the Pathogenesis and Treatment of Oral Inflammatory Diseases.

Dong Z, Wu L, Hong H Int J Mol Sci. 2023; 24(20).

PMID: 37895162 PMC: 10607498. DOI: 10.3390/ijms242015483.

-LPS Induces Mitochondrial Dysfunction Mediated by Neuroinflammation through Oxidative Stress.

Verma A, Azhar G, Zhang X, Patyal P, Kc G, Sharma S Int J Mol Sci. 2023; 24(2).

PMID: 36674463 PMC: 9861869. DOI: 10.3390/ijms24020950.

References

Shlossman M, Knowler W, Pettitt D, Genco R . Type 2 diabetes mellitus and periodontal disease. J Am Dent Assoc. 1990; 121(4):532-6. DOI: 10.14219/jada.archive.1990.0211. View

. The pathogenesis of periodontal diseases. J Periodontol. 1999; 70(4):457-70. DOI: 10.1902/jop.1999.70.4.457. View

Thatcher M, Tippetts T, Nelson M, Swensen A, Winden D, Hansen M . Ceramides mediate cigarette smoke-induced metabolic disruption in mice. Am J Physiol Endocrinol Metab. 2014; 307(10):E919-27. DOI: 10.1152/ajpendo.00258.2014. View

Offenbacher S, Jared H, OReilly P, Wells S, Salvi G, Lawrence H . Potential pathogenic mechanisms of periodontitis associated pregnancy complications. Ann Periodontol. 1998; 3(1):233-50. DOI: 10.1902/annals.1998.3.1.233. View

Scannapieco F, Bush R, Paju S . Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review. Ann Periodontol. 2004; 8(1):38-53. DOI: 10.1902/annals.2003.8.1.38. View

Taylor G, Burt B, Becker M, Genco R, Shlossman M, Knowler W . Severe Periodontitis and Risk for Poor Glycemic Control in Patients with Non-Insulin-Dependent Diabetes Mellitus. J Periodontol. 2018; 67 Suppl 10S:1085-1093. DOI: 10.1902/jop.1996.67.10s.1085. View

Fuggle N, Smith T, Kaul A, Sofat N . Hand to Mouth: A Systematic Review and Meta-Analysis of the Association between Rheumatoid Arthritis and Periodontitis. Front Immunol. 2016; 7:80. PMC: 4774606. DOI: 10.3389/fimmu.2016.00080. View

Beck J, Garcia R, Heiss G, Vokonas P, Offenbacher S . Periodontal disease and cardiovascular disease. J Periodontol. 1996; 67(10 Suppl):1123-37. DOI: 10.1902/jop.1996.67.10s.1123. View

Hansen M, Simmons K, Tippetts T, Thatcher M, Saito R, Hubbard S . Lipopolysaccharide Disrupts Mitochondrial Physiology in Skeletal Muscle via Disparate Effects on Sphingolipid Metabolism. Shock. 2015; 44(6):585-92. PMC: 4851226. DOI: 10.1097/SHK.0000000000000468. View

10.

Borges Jr I, Moreira E, Wilhem Filho D, de Oliveira T, da Silva M, Frode T . Proinflammatory and oxidative stress markers in patients with periodontal disease. Mediators Inflamm. 2008; 2007:45794. PMC: 2230499. DOI: 10.1155/2007/45794. View

11.

Beck J, Offenbacher S, Williams R, Gibbs P, Garcia R . Periodontitis: a risk factor for coronary heart disease?. Ann Periodontol. 1998; 3(1):127-41. DOI: 10.1902/annals.1998.3.1.127. View

12.

Cheng R, Choudhury D, Liu C, Billet S, Hu T, Bhowmick N . Gingival fibroblasts resist apoptosis in response to oxidative stress in a model of periodontal diseases. Cell Death Discov. 2016; 1:15046. PMC: 4979524. DOI: 10.1038/cddiscovery.2015.46. View

13.

Loos B . Systemic markers of inflammation in periodontitis. J Periodontol. 2005; 76(11 Suppl):2106-15. DOI: 10.1902/jop.2005.76.11-S.2106. View

14.

DAiuto F, Nibali L, Parkar M, Patel K, Suvan J, Donos N . Oxidative stress, systemic inflammation, and severe periodontitis. J Dent Res. 2010; 89(11):1241-6. PMC: 3318025. DOI: 10.1177/0022034510375830. View

15.

Chee B, Park B, Bartold P . Periodontitis and type II diabetes: a two-way relationship. Int J Evid Based Healthc. 2013; 11(4):317-29. DOI: 10.1111/1744-1609.12038. View

16.

Smith M, Tippetts T, Brassfield E, Tucker B, Ockey A, Swensen A . Mitochondrial fission mediates ceramide-induced metabolic disruption in skeletal muscle. Biochem J. 2013; 456(3):427-39. DOI: 10.1042/BJ20130807. View

17.

Eke P, Dye B, Wei L, Slade G, Thornton-Evans G, Borgnakke W . Update on Prevalence of Periodontitis in Adults in the United States: NHANES 2009 to 2012. J Periodontol. 2015; 86(5):611-22. PMC: 4460825. DOI: 10.1902/jop.2015.140520. View

18.

Paster B, Olsen I, Aas J, Dewhirst F . The breadth of bacterial diversity in the human periodontal pocket and other oral sites. Periodontol 2000. 2006; 42:80-7. DOI: 10.1111/j.1600-0757.2006.00174.x. View

19.

Power A, Pearson N, Pham T, Cheung C, Phillips A, Hickey A . Uncoupling of oxidative phosphorylation and ATP synthase reversal within the hyperthermic heart. Physiol Rep. 2014; 2(9). PMC: 4270237. DOI: 10.14814/phy2.12138. View

20.

Bullon P, Cordero M, Quiles J, Morillo J, Ramirez-Tortosa M, Battino M . Mitochondrial dysfunction promoted by Porphyromonas gingivalis lipopolysaccharide as a possible link between cardiovascular disease and periodontitis. Free Radic Biol Med. 2011; 50(10):1336-43. DOI: 10.1016/j.freeradbiomed.2011.02.018. View