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Review
. 2014 Jan 21;20(3):639-46.
doi: 10.3748/wjg.v20.i3.639.

Impairment of ghrelin synthesis in Helicobacter pylori-colonized stomach: new clues for the pathogenesis of H. pylori-related gastric inflammation

Omero Alessandro Paoluzi  1 , Del Vecchio Giovanna Blanco  1 , Roberta Caruso  1 , Ivan Monteleone  1 , Giovanni Monteleone  1 , Francesco Pallone  1
Affiliations
Review

Impairment of ghrelin synthesis in Helicobacter pylori-colonized stomach: new clues for the pathogenesis of H. pylori-related gastric inflammation

Omero Alessandro Paoluzi et al. World J Gastroenterol. .

Abstract

Ghrelin, the ligand of growth hormone secretagogue receptor 1a, takes part in several functions of the digestive system, including regulation of appetite, energy homeostasis, gastric acid secretion and motility. Ghrelin has also immunoregulatory properties and is supposed to inhibit some inflammatory pathways that can mediate gastric damage. Interestingly, ghrelin synthesis is reduced in the gastric mucosa of patients with Helicobacter pylori (H. pylori) infection, a worldwide condition inducing a T helper (Th)1/Th17 cell response-driven gastritis, which may evolve towards gastric atrophy and cancer. In this article, we review the available data on the expression of ghrelin in H. pylori infection and discuss how the defective ghrelin synthesis may contribute to sustain the ongoing inflammatory response in this disease.

Keywords: Gastritis; Ghrelin; Helicobacter pylori; T helper 1 cells.

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Figures

Figure 1
Figure 1
Main functions of ghrelin in the human body. INF: Interferon; IL: Interleukin; PGE2: Prostaglandin E2; Th1: T helper 1; APC: Antigen presenting cell.
Figure 2
Figure 2
Downregulation of ghrelin expression in the stomach during Helicobacter pylori infection. Epithelial damage and gastritis induced by Helicobacter pylori determine a diminished expression of ghrelin which, in turn, sustains the ongoing T helper (Th) 1 cells response. Down regulation of ghrelin is also followed by a reduced release of Prostaglandin E2 (PGE2) and interleukin (IL)-10 which, together with pro-inflammatory factors as IL-1β, contribute to the detrimental immune response and damage in the stomach. APC: Antigen presenting cell.
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