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

Helicobacter pylori is a Gram-negative bacterium affecting about half of th e world population, causing chronic gastritis type B dominated by activated phagocytes. In some patients the disease evolves into gastric ulcer, duode nal ulcer, gastric cancer or MALT lymphoma. The pathogenesis is in part cau sed by the immunological response. In mouse models and in human disease, th e 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 carotenoi ds and vitamin C may be an important factor for acquisition of H. pylori by humans. Dietary antioxidants may also affect both acquisition of the infec tion and the bacterial load of H. pylori infected mice. Antioxidants, inclu ding carotenoids, have anti-inflammatory effects. The aim of the present st udy was to investigate whether dietary antioxidant induced modulation of H. pylori in mice affected the cytokines produced by H. pylori specific T-cel ls. We found that treatment of H. pylori infected mice with an algal cell e xtract containing the antioxidant astaxanthin reduces bacterial load and ga stric inflammation. These changes are associated with a shift of the T-lymp hocyte 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. (C) 1999 Elsevier Science B.V. All rights res erved.