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      Helicobacter pylori infection is correlated with the incidence of erosive oral lichen planus and the alteration of the oral microbiome composition

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          Abstract

          Background

          Oral lichen planus (OLP), a common clinical oral disease, is associated with an increased risk of malignant transformation. The mechanism underlying the pathogenesis of OLP is unknown. Oral dysbacteriosis is reported to be one of the aetiological factors of OLP. Although Helicobacter pylori infection is associated with various oral diseases, the correlation between H. pylori infection and OLP is unclear. This study aimed to investigate the effect of H. pylori infection on OLP pathogenesis and oral microbiome composition in the Chinese population, which has a high incidence of H. pylori infection.

          Result

          In this study, saliva samples of 30 patients with OLP (OLP group) and 21 negative controls (NC group) were collected. H. pylori infection was detected using the carbon-13-labeled urea breath test (UBT). The saliva samples were divided into the following four groups based on the H. pylori status: H. pylori-positive OLP (OLP+), H. pylori-positive NC (NC+), H. pylori-negative OLP (OLP−), and H. pylori-negative NC (NC−). Oral microbiome compositions were significantly different between the OLP and NC groups and between the OLP− and OLP+ groups. Compared with those in the OLP− group, those in the OLP+ group had a higher incidence of erosive OLP and higher levels of salivary cytokines. In contrast, the oral microbiome composition and cytokine levels were not significantly different between the NC− and NC+ groups.

          Conclusions

          This is the first report to demonstrate that H. pylori infection is significantly correlated with the pathogenesis of erosive OLP.

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s12866-021-02188-0.

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          Most cited references48

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          Orexin activation counteracts decreases in nonexercise activity thermogenesis (NEAT) caused by high-fat diet.

          Overweight and obesity result from an imbalance between caloric intake and energy expenditure, including expenditure from spontaneous physical activity (SPA). Changes in SPA and resulting changes in non-exercise activity thermogenesis (NEAT) likely interact with diet to influence risk for obesity. However, previous research on the relationship between diet, physical activity, and energy expenditure has been mixed. The neuropeptide orexin is a driver of SPA, and orexin neuron activity can be manipulated using DREADDs (Designer Receptors Exclusively Activated by Designer Drugs). We hypothesized that HFD decreases SPA and NEAT, and that DREADD-mediated activation of orexin neuron signaling would abolish this decrease and produce an increase in NEAT instead. To test these ideas, we characterized behaviors to determine the extent to which access to a high-fat diet (HFD) influences the proportion and probability of engaging in food intake and activity. We then measured NEAT following access to HFD and following a DREADD intervention targeting orexin neurons. Two cohorts of orexin-cre male mice were injected with an excitatory DREADD virus into the caudal hypothalamus, where orexin neurons are concentrated. Mice were then housed in continuous metabolic phenotyping cages (Sable Promethion). Food intake, indirect calorimetry, and SPA were automatically measured every second. For cohort 1 (n=8), animals were given access to chow, then switched to HFD. For cohort 2 (n=4/group), half of the animals were given access to HFD, the other access to chow. Then, among animals on HFD, orexin neurons were activated following injections of clozapine n-oxide (CNO). Mice on HFD spent significantly less time eating (p<0.01) and more time inactive compared to mice on chow (p<0.01). Following a meal, mice on HFD were significantly more likely to engage in periods of inactivity compared to those on chow (p<0.05). NEAT was decreased in animals on HFD, and was increased to the NEAT level of control animals following activation of orexin neurons with DREADDs. Food intake (kilocalories) was not significantly different between mice on chow and HFD, yet mice on chow expended more energy per unit of SPA, relative to that in mice consuming HFD. These results suggest that HFD consumption reduces SPA and NEAT, and increases inactivity following a meal. Together, the data suggest a change in the efficiency of energy expenditure based upon diet, such that SPA during HFD burns fewer calories compared to SPA on a standard chow diet.
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            Insights into the human oral microbiome

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              Fifth Chinese National Consensus Report on the management of Helicobacter pylori infection.

              Since the 'Fourth Chinese National Consensus Report on the management of H. pylori infection' was published in 2012, three important consensuses (Kyoto global consensus report on H. pylori gastritis, The Toronto Consensus for the Treatment of H. pylori Infection in Adults and Management of H. pylori infection-the Maastricht V/Florence Consensus Report) have been published regarding the management of H. pylori infection.
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                Author and article information

                Contributors
                shaohuage@sdu.edu.cn
                syd@sdu.edu.cn
                Journal
                BMC Microbiol
                BMC Microbiol
                BMC Microbiology
                BioMed Central (London )
                1471-2180
                20 April 2021
                20 April 2021
                2021
                : 21
                : 122
                Affiliations
                [1 ]GRID grid.27255.37, ISNI 0000 0004 1761 1174, Key Laboratory for Experimental Teratology of Ministry of Education and Department of Microbiology, School of Basic Medical Science, , Cheeloo College of Medicine, Shandong University, ; Jinan, 250012 Shandong China
                [2 ]GRID grid.27255.37, ISNI 0000 0004 1761 1174, Department of Periodontology, School and Hospital of Stomatology, Cheeloo College of Medicine, , Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, ; Jinan, 250012 Shandong China
                [3 ]GRID grid.41156.37, ISNI 0000 0001 2314 964X, Department of Periodontology, Nanjing Stomatological Hospital, , Medical School of Nanjing University, ; 30 Zhongyang Road, Nanjing, 210008 China
                [4 ]GRID grid.27255.37, ISNI 0000 0004 1761 1174, Department of Implantology, School and Hospital of Stomatology, , Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, ; Jinan, Shandong People’s Republic of China
                [5 ]GRID grid.27255.37, ISNI 0000 0004 1761 1174, School of Medicine, Cheeloo College of Medicine, , Shandong University, ; Jinan, 250012 Shandong China
                Article
                2188
                10.1186/s12866-021-02188-0
                8059323
                33879055
                2750221d-de31-43c7-b908-ef4d3f46e4ef
                © The Author(s) 2021

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 24 December 2020
                : 7 April 2021
                Categories
                Research
                Custom metadata
                © The Author(s) 2021

                Microbiology & Virology
                helicobacter pylori,oral lichen planus,saliva,microbiome,inflammatory factor

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