astaxanthine and Gastritis

astaxanthine has been researched along with Gastritis* in 2 studies

Other Studies

2 other study(ies) available for astaxanthine and Gastritis

Article	Year
Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in Nutrients, 2018, Sep-18, Volume: 10, Issue:9 Topics: Adenosine Triphosphate; Antioxidants; Cell Line, Tumor; Epithelial Cells; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Host-Pathogen Interactions; Humans; Interleukin-8; Membrane Potential, Mitochondrial; Mitochondria; NF-kappa B; Oxidative Stress; PPAR gamma; Reactive Oxygen Species; Signal Transduction; Xanthophylls	2018
Treatment of H. pylori infected mice with antioxidant astaxanthin reduces gastric inflammation, bacterial load and modulates cytokine release by splenocytes. Immunology letters, 1999, Dec-01, Volume: 70, Issue:3 Helicobacter pylori is a gram-negative bacterium affecting about half of the world population, causing chronic gastritis type B dominated by activated phagocytes. In some patients the disease evolves into gastric ulcer, duodenal ulcer, gastric cancer or MALT lymphoma. The pathogenesis is in part caused by the immunological response. In mouse models and in human disease, the mucosal immune response is characterized by activated phagocytes. Mucosal T-lymphocytes are producing IFN-gamma thus increasing mucosal inflammation and mucosal damage. A low dietary intake of antioxidants such as carotenoids and vitamin C may be an important factor for acquisition of H. pylori by humans. Dietary antioxidants may also affect both acquisition of the infection and the bacterial load of H. pylori infected mice. Antioxidants, including carotenoids, have anti-inflammatory effects. The aim of the present study was to investigate whether dietary antoxidant induced modulation of H. pylori in mice affected the cytokines produced by H. pylori specific T-cells. We found that treatment of H. pylori infected mice with an algal cell extract containing the antioxidant astaxanthin reduces bacterial load and gastric inflammation. These changes are associated with a shift of the T-lymphocyte response from a predominant Th1-response dominated by IFN-gamma to a Th1/Th2-response with IFN-gamma and IL-4. To our knowledge, a switch from a Th1-response to a mixed Th1/Th2-response during an ongoing infection has not been reported previously. Topics: Animals; Antioxidants; beta Carotene; Cytokines; Gastritis; Helicobacter Infections; Helicobacter pylori; Interferon-gamma; Interleukin-4; Mice; Mice, Inbred BALB C; Spleen; T-Lymphocytes, Helper-Inducer; Xanthophylls	1999

Article

Year

Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in

Nutrients, 2018, Sep-18, Volume: 10, Issue:9

Topics: Adenosine Triphosphate; Antioxidants; Cell Line, Tumor; Epithelial Cells; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Host-Pathogen Interactions; Humans; Interleukin-8; Membrane Potential, Mitochondrial; Mitochondria; NF-kappa B; Oxidative Stress; PPAR gamma; Reactive Oxygen Species; Signal Transduction; Xanthophylls

2018

Treatment of H. pylori infected mice with antioxidant astaxanthin reduces gastric inflammation, bacterial load and modulates cytokine release by splenocytes.

Immunology letters, 1999, Dec-01, Volume: 70, Issue:3

Helicobacter pylori is a gram-negative bacterium affecting about half of the world population, causing chronic gastritis type B dominated by activated phagocytes. In some patients the disease evolves into gastric ulcer, duodenal ulcer, gastric cancer or MALT lymphoma. The pathogenesis is in part caused by the immunological response. In mouse models and in human disease, the mucosal immune response is characterized by activated phagocytes. Mucosal T-lymphocytes are producing IFN-gamma thus increasing mucosal inflammation and mucosal damage. A low dietary intake of antioxidants such as carotenoids and vitamin C may be an important factor for acquisition of H. pylori by humans. Dietary antioxidants may also affect both acquisition of the infection and the bacterial load of H. pylori infected mice. Antioxidants, including carotenoids, have anti-inflammatory effects. The aim of the present study was to investigate whether dietary antoxidant induced modulation of H. pylori in mice affected the cytokines produced by H. pylori specific T-cells. We found that treatment of H. pylori infected mice with an algal cell extract containing the antioxidant astaxanthin reduces bacterial load and gastric inflammation. These changes are associated with a shift of the T-lymphocyte response from a predominant Th1-response dominated by IFN-gamma to a Th1/Th2-response with IFN-gamma and IL-4. To our knowledge, a switch from a Th1-response to a mixed Th1/Th2-response during an ongoing infection has not been reported previously.

Topics: Animals; Antioxidants; beta Carotene; Cytokines; Gastritis; Helicobacter Infections; Helicobacter pylori; Interferon-gamma; Interleukin-4; Mice; Mice, Inbred BALB C; Spleen; T-Lymphocytes, Helper-Inducer; Xanthophylls

1999