Evodiamine Inhibits Helicobacter pylori Growth and Helicobacter pylori-Induced Inflammation

Yang, Ji Yeong; Kim, Jong-Bae; Lee, Pyeongjae; Kim, Sa-Hyun

doi:10.3390/ijms22073385

Cited by 31 publications

(20 citation statements)

References 68 publications

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“…Gastric epithelial cell line, AGS (Zhu et al, 2017;Yang et al, 2021), was obtained from the American Type Culture Collection (Manassas, VA, United States) and BGC-823 (Tang et al, 2013;Guo et al, 2020) was obtained from the Shanghai Institute CellBank, Chinese Academy of Sciences. The two cell lines were thawed and cultured in 3 ml of the complete Ham's F12 medium (1 × 10 5 cells/well) in a 12-well plate.…”

Section: Cell Linesmentioning

confidence: 99%

Cytotoxin-Associated Gene A-Negative Helicobacter pylori Promotes Gastric Mucosal CX3CR1+CD4+ Effector Memory T Cell Recruitment in Mice

Sun

et al. 2022

Front. Microbiol.

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BackgroundHelicobacter pylori can cause many kinds of gastric disorders, ranging from gastritis to gastric cancer. Cytotoxin-associated gene A (CagA)+H. pylori is more likely to cause gastric histopathologic damage than CagA–H. pylori. However, the underlying mechanism needs to be further investigated.Materials and methodsMice were intragastrically administered equal amounts of CagA+ or CagA–H. pylori. Four weeks later, 24 chemokines in stomachs were measured using a mouse chemokine array, and the phenotypes of the recruited gastric CD4+ T cells were analyzed. The migration pathway was evaluated. Finally, the correlation between each pair among the recruited CD4+ T cell sub-population, H. pylori colonization level, and histopathologic damage score were determined by Pearson correlation analysis.ResultsThe concentration of chemokines, CCL3 and CX3CL1, were significantly elevated in CagA–H. pylori-infected gastric mucosa than in CagA+H. pylori-infected gastric mucosa. Among them, CX3CL1 secreted by gastric epithelial cells, which was elicited more effectively by CagA–H. pylori than by the CagA+ strain, dramatically promoted mucosal CD4+ T cell migration. The expression of CX3CR1, the only known receptor of CX3CL1, was upregulated on the surface of gastric CD4+ T cells in CagA–H. pylori-infected stomach. In addition, most of the CX3CR1-positive gastric CD4+ T cells were CD44+CD69–CCR7– effector memory T cells (Tem). Pearson correlation analysis showed that the recruited CX3CR1+CD4+ Tem cell population was negatively correlated with H. pylori colonization level and histopathologic damage score.ConclusionCagA–H. pylori promotes gastric mucosal CX3CR1+CD4+ Tem recruitment in mice.

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Section: Cell Linesmentioning

confidence: 99%

Cytotoxin-Associated Gene A-Negative Helicobacter pylori Promotes Gastric Mucosal CX3CR1+CD4+ Effector Memory T Cell Recruitment in Mice

Sun

et al. 2022

Front. Microbiol.

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“…Studies have shown that the incidence of gastric cancer in whites is twice that of other races [29] . Long-term follow-up of the disasters in Hiroshima and Nagasaki Studies have shown that radiation has been identified as a high-risk risk factor for gastric cancer [30] . Early diagnosis of gastric cancer is still difficult worldwide and it is difficult to make a correct diagnosis under endoscopy in the early stage [14,31] .…”

Section: Resultsmentioning

confidence: 99%

Construction and Evaluation of Gastric Cancer Risk Prediction Model

Yang¹,

Long²,

Zhong³

et al. 2021

ijps

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To predict the probability of gastric cancer and precancerous lesions in patients and construct a risk model for gastric cancer based on related risk factors. 189 patients with gastric cancer or precancerous lesions diagnosed by pathological examination in our hospital from October 2016 to May 2021 were selected as the experimental group and 203 patients with chronic gastritis during the same period as the control group. Collect the clinical data of the two groups of patients use single factor analysis to screen and then perform multifactor logistic regression analysis. To predict the effect, the Hosmer-Lemeshow goodness-of-fit test evaluates its degree of fit. Univariate analysis showed body mass index, family history of gastric cancer, Helicobacter pylori infection, serum pepsinogen I/II ratio, gastrin 17, fruit and vegetable intake, age of recipients, physical activity and radiation work history in patients with gastric cancer and precancerous lesions. All were higher than the control group (p<0. 05). Logistic regression analysis showed thatHelicobacter pylori infection, serum pepsinogen I/II ratio and gastrin 17 were independent risk factors for gastric cancer. The area under curve of the prediction model constructed based on these three indicators is 0.924 (95 % CI: 0.891~0.993) and its sensitivity and specificity are 82.41 % and 94.93 %, respectively. The Hosmer-Lemeshow goodness-of-fit test result of the prediction model showed (Hosmer-Lemeshow c 2 =13.301, p=0.358), indicating that the prediction model has a good fit. Patients with Helicobacter pylori infection, serum pepsinogen I/II ratio and gastrin 17 are independent influencing factors. The prediction model established has good efficacy in predicting the risk of gastric cancer and precancerous lesions and can be used as a clinical guide for the prevention of gastric cancer.

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“…However, this mechanism needs to be further proved. In addition, studies have shown that VacA can also regulate mitogen-activated protein kinase pathway, phosphorylation of protein kinase B pathway, and autophagy, which also had relationship with inflammation and cell apoptosis [ 31–33 ]. Therefore, whether VacA can regulate other signaling pathways in lung injury remains to be further investigated.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori promotes inflammatory factor secretion and lung injury through VacA exotoxin-mediated activation of NF-κB signaling

et al. 2022

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Previous reports have shown that Helicobacter pylori ( H. pylori ) infection is associated with respiratory diseases. However, the pathogenesis remains unclear. Vacuolating cytotoxin A (VacA) is a major H. pylori exotoxin. In this study, we investigated the signaling pathways involved in the inflammatory response to H. pylori infection and VacA. Mice were treated with H. pylori and VacA, and histopathological analysis of lung tissues was performed using hematoxylin-eosin, Masson’s trichrome, and periodic acid Schiff staining. The secretion of inflammatory cytokines was evaluated by enzyme-linked immunosorbent assay. The expression of VacA, nuclear factor-kappa B (NF-κB), and p65 NF-κB was analyzed by Western blotting and immunofluorescence. Cell proliferation and apoptosis were assessed using the MTS assay and flow cytometry, respectively. In mice, H. pylori infection and VacA treatment promoted the secretion of the inflammatory factors interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), IL-6, and IL-8, increased p65 NF-κB protein phosphorylation, and induced lung injury. Furthermore, H. pylori infection promoted VacA production. In an in vitro cell model, VacA treatment significantly suppressed the proliferation of WI-38 and BEAS-2B cells, promoted apoptosis, induced TNF-α, IL-1β, IL-6, and IL-8 secretion, and promoted p65 NF-κB protein phosphorylation and NF-κB nuclear transfer. The NF-κB inhibitor BAY11-7082 alleviated VacA-induced inflammation and apoptosis and increased cell viability. In conclusion, VacA promotes the secretion of inflammatory factors and induces lung injury through NF-κB signaling.

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Evodiamine Inhibits Helicobacter pylori Growth and Helicobacter pylori-Induced Inflammation

Cited by 31 publications

References 68 publications

Cytotoxin-Associated Gene A-Negative Helicobacter pylori Promotes Gastric Mucosal CX3CR1+CD4+ Effector Memory T Cell Recruitment in Mice

Cytotoxin-Associated Gene A-Negative Helicobacter pylori Promotes Gastric Mucosal CX3CR1+CD4+ Effector Memory T Cell Recruitment in Mice

Construction and Evaluation of Gastric Cancer Risk Prediction Model

Helicobacter pylori promotes inflammatory factor secretion and lung injury through VacA exotoxin-mediated activation of NF-κB signaling

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