Curcumin inhibits gastric inflammation induced by Helicobacter pylori infection in a mouse model.

Elsa Seixas,Mónica Oleastro,Lucie Benejat,Paula Chaves,Jorge Machado,Pauline Floch,Teresa Lopes,Inês Gato,António Santos,Teresa Pereira,António Guerreiro

doi:10.3390/nu7010306

Abstract

Helicobacter pylori (H. pylori) infection triggers a sequence of gastric alterations starting with an inflammation of the gastric mucosa that, in some cases, evolves to gastric cancer. Efficient vaccination has not been achieved, thus it is essential to find alternative therapies, particularly in the nutritional field. The current study evaluated whether curcumin could attenuate inflammation of the gastric mucosa due to H. pylori infection. Twenty-eight C57BL/6 mice, were inoculated with the H. pylori SS1 strain; ten non-infected mice were used as controls. H. pylori infection in live mice was followed-up using a modified 13C-Urea Breath Test (13C-UBT) and quantitative real-time polymerase chain reaction (PCR). Histologically confirmed, gastritis was observed in 42% of infected non-treated mice at both 6 and 18 weeks post-infection. These mice showed an up-regulation of the expression of inflammatory cytokines and chemokines, as well as of toll-like receptors (TLRs) and MyD88, at both time points. Treatment with curcumin decreased the expression of all these mediators. No inflammation was observed by histology in this group. Curcumin treatment exerted a significant anti-inflammatory effect in H. pylori-infected mucosa, pointing to the promising role of a nutritional approach in the prevention of H. pylori induced deleterious inflammation while the eradication or prevention of colonization by effective vaccine is not available.

Highlights

Helicobacter pylori (H. pylori) is one of the most common human pathogens since it infects the gastric mucosa of about 50% of the world’s population [1]
H. pylori infection is a major risk factor for gastric cancer development because it triggers a stepwise sequence in the gastric mucosa starting with superficial gastritis, which can progress to chronic gastritis, atrophic gastritis, intestinal metaplasia, dysplasia, and, gastric carcinoma [3]
These results were confirmed by Quantitative Real-Time PCR (qPCR), for which no H. pylori DNA was detected among the noninfected mice, while no difference in H. pylori DNA content was observed between infected mice at 6 and 18 weeks, either treated or non-treated with curcumin (Figure 2)

Summary

Introduction

Helicobacter pylori (H. pylori) is one of the most common human pathogens since it infects the gastric mucosa of about 50% of the world’s population [1]. Epidemiological studies associating the infection with a higher risk of gastric malignancy lead the World Health Organization for Research in Cancer to classify. H. pylori infection is a major risk factor for gastric cancer development because it triggers a stepwise sequence in the gastric mucosa starting with superficial gastritis, which can progress to chronic gastritis, atrophic gastritis, intestinal metaplasia, dysplasia, and, gastric carcinoma [3]. The bacteria induce a host immune response (innate and adaptative), but the persistence of the infection suggests that the response is not effective in eliminating the infection. Multiple lines of evidence suggest that the immune response contributes to the pathogenesis associated with the infection

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Conclusion