Effect of Helicobacter pylori infection on chronic periodontitis by the change of microecology and inflammation
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Zhekai Hu1, Yu Zhang1, Zhiyu Li2, Yuedi Yu3,4, Wenyan Kang1,5, Yingnan Han2, Xiwen Geng2, Shaohua Ge1,5, Yundong Sun2
1Shandong Provincial Key Laboratory of Oral Tissue Regeneration, School of Stomatology, Shandong University, Jinan, Shandong 250012, People’s Republic of China
2Department of Microbiology, Key Laboratory for Experimental Teratology of Chinese Ministry of Education, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
3Shanghai Southwest Weiyu Middle School, Shanghai 200233, People’s Republic of China
4Laboratory of Oral Tumor Biology, Shanghai Research Institute of Stomatology Ninth People Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, People’s Republic of China
5Department of Periodontology, School of Stomatology, Shandong University, Jinan, Shandong 250012, People’s Republic of China
Shaohua Ge, email: [email protected]
Yundong Sun, email: [email protected]
Keywords: Helicobacter pylori, Wnt5a, IL-8, chronic periodontitis, inflammation
Received: April 30, 2016 Accepted: August 11, 2016 Published: August 20, 2016
Helicobacter pylori (H. pylori), a pathogen inducing peptic disease, is recently found to be binding to the progress of periodontitis. Most previous studies are case-controlled, and they investigate the risk of H. pylori infection in disease the development of while few studies evaluate the correlation between H. pylori and periodontal pathogens. Therefore, we investigated the correlation between H. pylori infection with periodontal parameters, periodontal pathogens and inflammation. The results indicated that patients with H. pylori showed significantly higher probing depth and attachment loss than those without (p < 0.05). Among 28 subgingival plaque samples from 14 patients, the frequencies of Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum and Treponema denticola were significantly higher with H. pylori infection than those without H. pylori infection (p < 0.05). However, the frequency of Aggregatibacter actinomycetemcomitans was lower (p < 0.05). Furthermore, after human acute monocytic leukemia cell line (THP-1) was stimulated with cagA-positive standard strains (cagA+ H. pylori 26695), the expression of periodontitis-related molecules Wnt5a, interleukin 8 (IL-8), interleukin 6 (IL-6) and interferon gamma (IFN-γ) significantly increased (p < 0.05). Conversely, the expression of tumor necrosis factor alpha (TNF-α) was almost stable. Meanwhile, cagA+ H. pylori promoted significantly higher expression of IL-8 and Wnt5a than isogenic cagA mutants strains (cagA− H. pylori 26695) did. Taken together, our data suggested that H. pylori might promote the growth of some periodontal pathogens and aggravate the progress of chronic periodontitis.
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