Elevated Levels of Interferon-<i>γ</i> Are Associated with High Levels of Epstein-Barr Virus Reactivation in Patients with the Intestinal Type of Gastric Cancer

Cárdenas-Mondragón, María G.; Torres, Javier; Sánchez-Zauco, Norma; Gómez‐Delgado, Alejandro; Camorlinga‐Ponce, Margarita; Maldonado‐Bernal, Carmen; Fuentes‐Pananá, Ezequiel M.

doi:10.1155/2017/7069242

Cited by 16 publications

(18 citation statements)

References 46 publications

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“…However, no significant difference was present between the two groups (P = 0.414). Another study showed that IFN-γ was associated with high levels of EBV reactivation in patients with gastric cancer [18]. Similarly, our study confirmed that IL-10 and IFN-γ concentrations were positively correlated with the EBV-DNA copy number in peripheral blood.…”

Section: Discussionsupporting

confidence: 87%

T-lymphocyte subsets and Th1/Th2 cytokines in convalescent patients with Epstein–Barr virus-associated aplastic anemia

Chen

Bao

et al. 2019

Hematology

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Objective: The aim of this study was to analyze T-lymphocyte subsets and Th1/Th2 cytokines in convalescent patients with Epstein-Barr virus (EBV)-associated aplastic anemia (AA). Methods: Sixty AA patients were enrolled, who were in remission following immunosuppressive therapy, including 34 EBV-negative cases and 26 EBV-positive cases. Their complete blood count (CBC), T-lymphocyte subsets, Th1/Th2 cytokines were analyzed. The correlation between EBV-DNA and T-lymphocyte subsets was evaluated, as well as the relationship between EBV-DNA and Th1/Th2 cytokines. The presence of EBV-DNA in peripheral blood mononuclear cells (PBMCs) was also assessed in 60 normal controls. Results: EBV-DNA was detected in 26/60 (43.33%) patients and 21/60 (35.00%) controls. EBV-DNA copy number in AA patients was higher than in controls (Z = −2.138, P = 0.033). The percentage of CD3 + CD4 + T-lymphocytes and the ratio of CD4 + /CD8 + T-lymphocytes in the EBV-negative group were higher than in the EBV-positive group (P = 0.001 and 0.001, respectively). EBV was positively correlated with CD3 + CD8 + T-lymphocyte percentages (Pearson R: 0.496, P = 0.009). Moreover, EBV was positively correlated with IL-10 and IFN-γ levels (Pearson R: 0.559, P = 0.002 and Pearson R: 0.621, P = 0.001, respectively). Conclusions: EBV-DNA copy number in AA patients was higher than in normal controls. Both AA and EBV infection may cause changes in the levels of T-lymphocyte subsets. We recommend monitoring the changes in the immune function and EBV infection simultaneously in AA patients, especially following immunosuppressive therapy.

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Section: Discussionsupporting

confidence: 87%

T-lymphocyte subsets and Th1/Th2 cytokines in convalescent patients with Epstein–Barr virus-associated aplastic anemia

Chen

Bao

et al. 2019

Hematology

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“…For example, interferon γ (IFN-γ) secretion induced by H. pylori promotes an inflammatory milieu that exacerbates disease severity [29], and this cytokine, along with IL-6 and IL-13, promote EBV proliferation, and higher levels of proinflammatory cytokines, including IL-1β, tumor necrosis factor α (TNF-α) and IL-8, have been reported to promote severe gastritis associated EBV and H. pylori Pathogens 2020, 9, 104 4 of 17 co-infection [10]. In line with these observations, IFN-γ levels in the plasma of patients with gastric cancers are positively correlated with the degree of EBV reactivation [30].…”

Section: Biology and Disease Associations Of H Pylori And Ebvmentioning

confidence: 74%

Epstein–Barr Virus and Helicobacter Pylori Co-Infection in Non-Malignant Gastroduodenal Disorders

Dávila-Collado¹,

Jarquín-Durán²,

Dong

et al. 2020

Pathogens

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Epstein–Barr virus (EBV) and Helicobacter pylori (H. pylori) are two pathogens associated with the development of various human cancers. The coexistence of both microorganisms in gastric cancer specimens has been increasingly reported, suggesting that crosstalk of both pathogens may be implicated in the carcinogenesis process. Considering that chronic inflammation is an initial step in the development of several cancers, including gastric cancer, we conducted a systematic review to comprehensively evaluate publications in which EBV and H. pylori co-infection has been documented in patients with non-malignant gastroduodenal disorders (NMGDs), including gastritis, peptic ulcer disease (PUD), and dyspepsia. We searched the PubMed database up to August 2019, as well as publication references and, among the nine studies that met the inclusion criteria, we identified six studies assessing EBV infection directly in gastric tissues (total 949 patients) and three studies in which EBV infection status was determined by serological methods (total 662 patients). Due to the substantial methodological and clinical heterogeneity among studies identified, we could not conduct a meta-analysis. The overall prevalence of EBV + H. pylori co-infection in NMGDs was 34% (range 1.8% to 60%). A higher co-infection rate (EBV + H. pylori) was reported in studies in which EBV was documented by serological methods in comparison with studies in which EBV infection was directly assessed in gastric specimens. The majority of these studies were conducted in Latin-America and India, with most of them comparing NMGDs with gastric cancer, but there were no studies comparing the co-infection rate in NMGDs with that in asymptomatic individuals. In comparison with gastritis caused by only one of these pathogens, EBV + H. pylori co-infection was associated with increased severity of gastric inflammation. In conclusion, only relatively small studies testing EBV and H. pylori co-infection in NMGDs have been published to date and the variable report results are likely influenced by geographic factors and detection methods.

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“…EBV remains latent after infection and does not immediately exhibit pathogenicity. Lytic replication of EBV induces an inflammatory reaction involving the expression of inflammatory mediators, such as interleukin‐1β, interferon‐γ and Toll‐like receptors (Cárdenas‐Mondragón et al , Farina et al , Torii et al ). Thus, reactivation of EBV may be associated with the onset of disease.…”

Section: Introductionmentioning

confidence: 99%

Epstein–Barr virus reactivation by persistent apical periodontal pathogens

et al. 2019

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Aim To assess whether Epstein–Barr virus (EBV) reactivation is triggered by persistent apical periodontitis‐related microbes using in vitro and ex vivo methodologies. Methodology Surgically removed human periapical granulomas (n = 50) and healthy gingival tissues (n = 10) were analysed to determine the presence of EBV and seven persistent apical periodontitis‐related microbes. In addition, real‐time polymerase chain reaction was used to detect the mRNA expression of BZLF‐1, an immediate–early gene of EBV. Expression of latent membrane protein (LMP)‐1 and ZEBRA, an early lytic protein of EBV encoded by BZLF‐1, was also examined using triple‐colour immunofluorescence staining. n‐Butyric acid produced by the microbes was quantified, and luciferase assays were performed in association with bacterial lysates. In addition, Daudi cells were cultured with bacterial lysates, and the expression levels of BZLF‐1 mRNA and ZEBRA protein were determined. Results EBV DNA and BZLF‐1 mRNA were detected in 47 out of 50 periapical granulomas, but not in healthy gingival tissues. The EBV DNA copy number and the number of Fusobacterium nucleatum were significantly positively correlated with BZLF‐1 expression in periapical granulomas. The number of Prevotella intermedia was slightly correlated with BZLF‐1 expression; however, the other microbes were not. CD79a‐positive B cells in periapical granulomas, but not those in healthy gingival tissues, expressed both LMP‐1 and ZEBRA. n‐Butyric acid production was the highest in F. nucleatum and the lowest in P. intermedia. Enterococcus faecalis, Candida albicans and the other tested microbes did not produce n‐butyric acid. An F. nucleatum lysate exhibited significantly increased BZLF‐1‐luciferase activity in the same manner of commercial butyric acid, whereas P. intermedia did not. F. nucleatum also induced the expression of BZLF‐1 mRNA and ZEBRA protein by Daudi cells, indicating that EBV reactivation was induced. Conclusion Among the persistent apical periodontitis‐related bacteria that were tested, F. nucleatum most strongly reactivated latent EBV, whereas E. faecalis and C. albicans as well as the other microbes did not.

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Elevated Levels of Interferon-γ Are Associated with High Levels of Epstein-Barr Virus Reactivation in Patients with the Intestinal Type of Gastric Cancer

Cited by 16 publications

References 46 publications

T-lymphocyte subsets and Th1/Th2 cytokines in convalescent patients with Epstein–Barr virus-associated aplastic anemia

T-lymphocyte subsets and Th1/Th2 cytokines in convalescent patients with Epstein–Barr virus-associated aplastic anemia

Epstein–Barr Virus and Helicobacter Pylori Co-Infection in Non-Malignant Gastroduodenal Disorders

Epstein–Barr virus reactivation by persistent apical periodontal pathogens

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