title: Mitochondrial dysfunction promoted by Porphyromonas gingivalis lipopolysaccharide as a possible link between cardiovascular disease and periodontitis.
abstract: Oxidative stress is one of the factors that could explain the pathophysiological mechanism of inflammatory conditions that occur in cardiovascular disease (CVD) and periodontitis. Such inflammatory response is often evoked by specific bacteria, as the lipopolysaccharide (LPS) of Porphyromonas gingivalis is a key factor in this process. The aim of this research was to study the role of mitochondrial dysfunction in peripheral blood mononuclear cells (PBMCs) from periodontitis patients and to evaluate the influence of LPS on fibroblasts to better understand the pathophysiology of periodontitis and its relationship with CVD. PBMCs from patients showed lower CoQ10 levels and citrate synthase activity, together with high levels of ROS production. LPS-treated fibroblasts provoked increased oxidative stress and mitochondrial dysfunction by a decrease in mitochondrial protein expression, mitochondrial mass, and mitochondrial membrane potential. Our study supports the hypothesis that LPS-mediated mitochondrial dysfunction could be at the origin of oxidative stress in periodontal patients. Abnormal PBMC performance may promote oxidative stress and alter cytokine homeostasis. In conclusion, mitochondrial dysfunction could represent a possible link to understanding the interrelationships between two prominent inflammatory diseases: periodontitis and CVD.
authors.affiliation: Department of Periodontology, Dental School, University of Sevilla, Sevilla, Spain.
authors.forename: Pedro
authors.initials: P
authors.lastname: Bullon
authors.forename: Mario David
authors.initials: MD
authors.lastname: Cordero
authors.forename: José Luis
authors.initials: JL
authors.lastname: Quiles
authors.forename: Juan Manuel
authors.initials: JM
authors.lastname: Morillo
authors.forename: Maria
authors.initials: M
authors.lastname: del Carmen Ramirez-Tortosa
authors.forename: Maurizio
authors.initials: M
authors.lastname: Battino
mesh_terms: D000328:Adult; D017209:Apoptosis / Q000187:drug effects; D002318:Cardiovascular Diseases / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology*; D005347:Fibroblasts / Q000187:drug effects / Q000276:immunology; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008875:Middle Aged; D008928:Mitochondria / Q000187:drug effects* / Q000276:immunology; D018384:Oxidative Stress / Q000187:drug effects; D010518:Periodontitis / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology*; D016966:Porphyromonas gingivalis / Q000737:chemistry* / Q000302:isolation & purification; D017382:Reactive Oxygen Species / Q000276:immunology
chemical_list: D008070:Lipopolysaccharides; D017382:Reactive Oxygen Species