Astaxanthin from Shrimp Cephalothorax Stimulates the Immune Response by Enhancing IFN-γ, IL-10, and IL-2 Secretion in Splenocytes of <i>Helicobacter Pylori</i>-Infected Mice

Infection with <i>Helicobacter pylori</i> is a critical cause of gastrointestinal diseases. A crucial host response associated with <i>H. pylori</i> infection includes gastric inflammation, which is characterized by a sustained recruitment of T-helper (Th) cells to the site o...

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Bibliographic Details
Main Authors: Sergio Davinelli, Heidi Mikkelsen Melvang, Leif Percival Andersen, Giovanni Scapagnini, Michael Engelbrecht Nielsen
Format: Article
Language:English
Published: MDPI AG 2019-06-01
Series:Marine Drugs
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Online Access:https://www.mdpi.com/1660-3397/17/7/382
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Summary:Infection with <i>Helicobacter pylori</i> is a critical cause of gastrointestinal diseases. A crucial host response associated with <i>H. pylori</i> infection includes gastric inflammation, which is characterized by a sustained recruitment of T-helper (Th) cells to the site of infection and distinct patterns of cytokine production. Adequate nutritional status, especially frequent consumption of dietary antioxidants, appears to protect against infection with <i>H. pylori</i>. The aim of the present study was to investigate whether astaxanthin (AXT) from shrimp cephalothorax may modulate cytokine release of splenocytes in <i>H. pylori</i>-infected mice (<i>n</i> = 60). Six- to eight-week-old female mice were divided into three groups (<i>n</i> = 20 per group) to receive a daily oral dose of 10 or 40 mg of AXT for six weeks. After six weeks, a trend toward interferon gamma (IFN-&#947;) upregulation was found (40 mg; <i>p</i> &lt; 0.05) and a significant dose-dependent increase of interleukin 2 (IL-2) and IL-10 (both <i>p</i> &lt; 0.05) was observed. These results suggest that AXT induces higher levels of IL-2 and a shift to a balanced Th1/Th2 response by increasing IFN-&#947; and augmenting IL-10. We concluded that AXT may influence the pattern of cytokines during <i>H. pylori</i> infection.
ISSN:1660-3397