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

Davinelli Davinelli,Nielsen Nielsen,Melvang Melvang,Scapagnini Scapagnini,Andersen Andersen

doi:10.3390/md17070382

Abstract

Infection with Helicobacter pylori is a critical cause of gastrointestinal diseases. A crucial host response associated with H. pylori 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 H. pylori. The aim of the present study was to investigate whether astaxanthin (AXT) from shrimp cephalothorax may modulate cytokine release of splenocytes in H. pylori-infected mice (n = 60). Six- to eight-week-old female mice were divided into three groups (n = 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-γ) upregulation was found (40 mg; p < 0.05) and a significant dose-dependent increase of interleukin 2 (IL-2) and IL-10 (both p < 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-γ and augmenting IL-10. We concluded that AXT may influence the pattern of cytokines during H. pylori infection.

Highlights

Helicobacter pylori is a gram-negative bacterium that infects more than half of the world’s population [1]
Long-term gastric inflammation is the hallmark of chronic H. pylori infection and is thought to underlie several gastrointestinal diseases
The inflammation of the gastric mucosa depends mainly on T-helper 1 (Th1) cell responses, it has been acknowledged that H. pylori infection induces the differentiation of anti-inflammatory

Summary

Introduction

Helicobacter pylori is a gram-negative bacterium that infects more than half of the world’s population [1]. H. pylori colonization usually occurs in childhood and persists throughout life, causing chronic gastritis, peptic ulceration, gastric adenocarcinoma, and primary gastric lymphoma [2]. Long-term gastric inflammation is the hallmark of chronic H. pylori infection and is thought to underlie several gastrointestinal diseases. The severity of gastric inflammation varies, depending on the host immune response against this bacterium. Colonization by H. pylori recruits host immune system cells such as macrophages, neutrophils, and lymphocytes to the gastric mucosa [3,4]. The inflammation of the gastric mucosa depends mainly on T-helper 1 (Th1) cell responses, it has been acknowledged that H. pylori infection induces the differentiation of anti-inflammatory

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