Abstract
The anti-inflammatory and antimicrobial properties of curcumin suggest its use as an anti-Helicobacter pylori (H. pylori) agent, but mechanisms underlying its helpful activity are still not clear. Indoleamine 2,3-dioxygenase (IDO) promotes the effector T cell apoptosis by catalyzing the rate-limiting first step in tryptophan catabolism, and its high expression in H. pylori-infected human gastric mucosa attenuates Th1 and Th17 immune response. The aim of this study was to investigate the role of curcumin in modulating the expression of IL-17 and IDO in H. pylori-infected human gastric mucosa. In an organ culture chamber, gastric biopsies from 35 patients were treated with and without 200 μM curcumin. In H. pylori-infected patients (n = 21), IL-17 was significantly lower, both in gastric biopsies (p = 0.0003) and culture supernatant (p = 0.0001) while IDO significantly increased (p < 0.00001) in curcumin-treated sample compared with untreated samples. In a subgroup of H. pylori-infected patients (n = 15), samples treated with curcumin in addition to IDO inhibitor 1-methyl-L-tryptophan (1-MT) showed a higher expression of IL-17 compared with untreated samples and curcumin-treated alone (p < 0.00001). Curcumin downregulates IL-17 production through the induction of IDO in H. pylori-infected human gastric mucosa, suggesting its role in dampening H. pylori-induced immune-mediated inflammatory changes.
Highlights
Helicobacter pylori (H. pylori) is a ubiquitous pathogen, and it is believed that at least 50% of the world’s population has been infected [1]
To evaluate the ability of curcumin to dampen the mucosal inflammation in human gastric mucosa, we measured the expression of the proinflammatory cytokine IL-17 in gastric tissue and its ABABAB IL-17
Levels of IL-17 resulted significantly lower in curcumin-treated sample compared with untreated samples, both in gastric biopsies (0.56 ± 0.15 arbitrary units (a.u.) vs. 0.80 ± 0.19 a.u., p = 0 0003, Figure 1) and culture supernatant (25.18 ± 10.77 pg/mL vs. 40.66 ± 11.69 pg/mL, p = 0 0001, Figure 2) from H. pylori-infected patients (n = 21)
Summary
Helicobacter pylori (H. pylori) is a ubiquitous pathogen, and it is believed that at least 50% of the world’s population has been infected [1]. The epidemiology of H. pylori infection is undergoing changes with regard to improvements in hygienic and socioeconomic conditions and most infections remain asymptomatic, there are few prospective studies in the general population, despite the infection still having a major impact on public health [2]. The human host mounts an innate and adaptive immune responses against the bacterium, but this is not enough to clear the infection [4]. H. pylori is able to manipulate the responses of the T helper cells and their signature cytokines, avoiding its clearance by the host immune system [5]. Th1 polarization occurring during H. pylori infection is well documented, but evidences suggest its modulation by the bacterium, which in this way allows the persistence of the infection and the development of H. pylori-related burden of diseases [6]
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