Porphyromonas gingivalis infection reduces regulatory T cells in infected atherosclerosis patients.
Increasing evidence has shown periodontal pathogen Porphyromonas gingivalis (P.gingivalis) infection contributes to atherosclerosis (AS) progression. P.gingivalis fimbriae act as an important virulence factor in AS. Regulatory T cells (Tregs) may play a crucial role in autoimmune response during this process. However, whether P.gingivalis infection is associated with Tregs dysregulation during AS is still unknown and the prevalence of different P.gingivalis FimA genotypes during this process is unclear. Here we analyzed the distribution of Tregs and in P.gingivalis-infected atherosclerotic patients to reveal the relationship between P.gingivalis infection and Tregs reduction/dysfunction and to elucidate their role in periodontitis-AS interaction. FimA genotype was also examined to determine the prevalence of fimbriae. Our results showed that P.gingivalis infection reduced Tregs in atherosclerotic patients compared with non-atherosclerotic patients and health controls. Concentration of TGF-β1, which plays an important role in the development of Tregs, also decreased in P.gingivalis infected patients. Furthermore, type II FimA seems to show higher prevalence than the other five detected types. The population of Tregs further decreased in patients with type II FimA compared with the other types. P.gingivlias FimA genotype II was the dominant type associated with decreased Treg population. These results indicate that P.gingivalis infection may be associated with Tregs dysregulation in AS; type II FimA may be a predominant genotype in this process.
Department of Periodontology, Hospital of Stomatology, Medical School, Nanjing University, Nanjing, Jiangsu Province, China ; Central Laboratory of Stomatology, Hospital of Stomatology, Medical School, Nanjing University, Nanjing, Jiangsu Province, China.
Jie
J
Yang
Department of Periodontology, Hospital of Stomatology, Medical School, Nanjing University, Nanjing, Jiangsu Province, China.
Juan
J
Wu
Department of Periodontology, Hospital of Stomatology, Medical School, Nanjing University, Nanjing, Jiangsu Province, China.
Yu
Y
Liu
Department of Cardiology, Nanjing Chest Hospital, Nanjing, Jiangsu Province, China.
Jin
J
Huang
Department of Cardiology, Nanjing Chest Hospital, Nanjing, Jiangsu Province, China.
Zhipin
Z
Lu
Key Laboratory of Cardiovascular Disease and Molecular Intervention, Atherosclerosis Research Centre, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Liping
L
Xie
Department of Periodontology, Hospital of Stomatology, Medical School, Nanjing University, Nanjing, Jiangsu Province, China.
Weibin
W
Sun
Key Laboratory of Cardiovascular Disease and Molecular Intervention, Atherosclerosis Research Centre, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Yong
Y
Ji
D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D050197:Atherosclerosis / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D016866:Bacteroidaceae Infections / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D010861:Fimbriae, Bacterial / Q000473:pathology*; D005434:Flow Cytometry; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D008297:Male; D008875:Middle Aged; D010518:Periodontitis / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D016966:Porphyromonas gingivalis / Q000302:isolation & purification*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000097:blood
D000907:Antibodies, Bacterial; D007074:Immunoglobulin G; D053773:Transforming Growth Factor beta1