Abstract:Marina crystal minerals (MCM) are a mixture that contains crystallized minerals
along with trace elements extracted from seawater. It is a nutritional
supplement that is capable of enhancing natural killer (NK) cell activity and
increasing T and B cell proliferation in humans post ingestion. However, its
effect on dendritic cells (DCs), the cells that bridge innate and adaptive
immunity, is not yet known. In this study, we examine the stimulatory effects of
MCM on DCs’ maturation and function in vitro. Human m… Show more
“…pylori infection in mice, and further research on gastric carcinoma in situ will be conducted in future studies. Studies have shown that dendritic cells can stimulate CD4 + T to secrete a large amount of interferon (IFN‐γ) and stimulate CD8 + T cells to express higher levels of CD107a 47 . Moreover, mature DCs may enhance the infiltration of CD8 + T and CD4 + T cells into cancer cells 48‐50 …”
Background: Recent studies and clinical samples have demonstrated that Helicobacter pylori could induce the downregulation of miR-375 in the stomach and promote gastric carcinogenesis. However, whether the immune cells are affected by Helicobacter pylori due to the downregulation of miR-375 is unclear.
Materials and methods:In this study, we constructed an overexpression and knockdown of miR-375 and Helicobacter pylori infection cell models in vitro. In addition, the maturity of dendritic cells (DCs) and the expression of IL-6, IL-10, and VEGF at the transcriptional and translational levels were analyzed. Changes in the JAK2-STAT3 signaling pathway were detected. In vivo, the number changes in CD4+ T and CD8+ T cells and the size changes of tumors via models of transplantable subcutaneous tumors were also analyzed.
Results: A cell model of Helicobacter pylori and gastric cancer was used to identify the expression of miR-375 and the maturity of dendritic cells. This study found that Helicobacter pylori could downregulate miR-375, which regulates the expression of cytokines IL-6, IL-10, and VEGF in the stomach. MiR-375 regulated the expression of cytokines IL-6, IL-10, and VEGF through the JAK2-STAT3 signaling pathway in vitro. In addition, we found that Helicobacter pylori regulates the maturation of dendritic cells through miR-375. These results were further verified in vivo, and miR-375 diminishes tumor size was also demonstrated. This study showed that immature DCs caused a decrease in the number of CD4+ and CD8+ T cells. Conclusions: This study demonstrated that Helicobacter pylori can inhibit miRNA-375 expression in the stomach. Downregulated miR-375 activates the JAK2-STAT3 pathway. Activating the JAK2-STAT3 signaling pathway promotes the secretion of IL-6, IL-10, and VEGF, leading to immature differentiation of DCs and induction of gastric cancer.
“…pylori infection in mice, and further research on gastric carcinoma in situ will be conducted in future studies. Studies have shown that dendritic cells can stimulate CD4 + T to secrete a large amount of interferon (IFN‐γ) and stimulate CD8 + T cells to express higher levels of CD107a 47 . Moreover, mature DCs may enhance the infiltration of CD8 + T and CD4 + T cells into cancer cells 48‐50 …”
Background: Recent studies and clinical samples have demonstrated that Helicobacter pylori could induce the downregulation of miR-375 in the stomach and promote gastric carcinogenesis. However, whether the immune cells are affected by Helicobacter pylori due to the downregulation of miR-375 is unclear.
Materials and methods:In this study, we constructed an overexpression and knockdown of miR-375 and Helicobacter pylori infection cell models in vitro. In addition, the maturity of dendritic cells (DCs) and the expression of IL-6, IL-10, and VEGF at the transcriptional and translational levels were analyzed. Changes in the JAK2-STAT3 signaling pathway were detected. In vivo, the number changes in CD4+ T and CD8+ T cells and the size changes of tumors via models of transplantable subcutaneous tumors were also analyzed.
Results: A cell model of Helicobacter pylori and gastric cancer was used to identify the expression of miR-375 and the maturity of dendritic cells. This study found that Helicobacter pylori could downregulate miR-375, which regulates the expression of cytokines IL-6, IL-10, and VEGF in the stomach. MiR-375 regulated the expression of cytokines IL-6, IL-10, and VEGF through the JAK2-STAT3 signaling pathway in vitro. In addition, we found that Helicobacter pylori regulates the maturation of dendritic cells through miR-375. These results were further verified in vivo, and miR-375 diminishes tumor size was also demonstrated. This study showed that immature DCs caused a decrease in the number of CD4+ and CD8+ T cells. Conclusions: This study demonstrated that Helicobacter pylori can inhibit miRNA-375 expression in the stomach. Downregulated miR-375 activates the JAK2-STAT3 pathway. Activating the JAK2-STAT3 signaling pathway promotes the secretion of IL-6, IL-10, and VEGF, leading to immature differentiation of DCs and induction of gastric cancer.
“…Our previous work has shown that Biobran/MGN-3 (an arabinoxylan rice bran), PFT (a novel kefir product), and Marina Crystal Minerals (MCM; a mixture of crystallized minerals and trace elements extracted from seawater) all promote the production of inflammatory and anti-inflammatory cytokines. 27,31,32 Biobran and PFT also stimulate DC-primed CD4+ T cell proliferation and their production of IL-10, and MCM causes the upregulation of co-stimulatory molecules CD86, CD80, and HLA-DR. In addition, DPV576 (a dispersed aqueous mixture composed of nanodiamond and nanoplatinum) activates human DCs and upregulates the levels of DC-secreted cytokine IL-10, 33 and we have recently observed that exposure of human CD4+ T lymphocytes to DPV576 inhibits the activity of the transient receptor potential vanilloid channel TRPV1 in CD4+ T lymphocytes, suggesting that it has the potential for use in pain management.…”
The hydroferrate fluid MRN-100, an iron-based compound with potent antioxidant characteristics, was examined to identify its possible anti-inflammatory effects on human dendritic cells (DCs) in vitro. Human monocyte-derived DCs were treated with MRN-100 at two concentrations (50 and 100 μL/mL) for 24 h and then stimulated with or without lipopolysaccharides (LPS). The expression of DC maturation markers was assessed by flow cytometry and the production of cytokines was determined by enzyme-linked immunosorbent assay (ELISA). Functional assay was performed by coculturing MRN-100-treated and untreated DCs with allogeneic naïve CD4+ T cells and assaying the T cells' cytokine production. Results show that treatment with MRN-100 significantly upregulated the co-stimulatory molecules CD80 and CD86 and increased human leukocyte antigen-DR (HLA-DR) though not significantly. MRN-100 treatment also significantly increased the production of the anti-inflammatory cytokine interleukin (IL)-10. On the other hand, MRN-100 significantly induced the secretion of pro-inflammatory cytokines such as IL-6 only at high concentrations. Furthermore, DCs pretreated with MRN-100 and either stimulated or not with LPS were able to prime CD4+ T cells to secrete significant amounts of IL-10 while inhibiting the secretion of pro-inflammatory cytokine tumor necrosis factor (TNF)-α. These results indicate that MRN-100 is a powerful anti-inflammatory agent that promotes the generation of an antiinflammatory immune response in vitro. MRN-100 could be beneficial for treating patients with inflammatory diseases, including arthritis and type 1 diabetes, and its potential benefits should be examined in clinical trials.
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