Enhanced Expression of Indoleamine 2,3‐Dioxygenase in <i>Helicobacter pylori</i>‐Infected Human Gastric Mucosa Modulates Th1/Th2 Pathway and Interleukin 17 Production

Larussa, Tiziana; Leone, Isabella; Suraci, Evelina; Nazionale, Immacolata; Procopio, Teresa; Conforti, Francesco; Abenavoli, Ludovico; Hribal, Marta Letizia; Imeneo, Maria; Luzza, Francesco

doi:10.1111/hel.12174

Cited by 27 publications

(27 citation statements)

References 31 publications

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“…Very recent data from analyses performed on gastric biopsy samples from human patients suggest an immune-modulatory and protective action of IDO1 against gastritis in H. pylori subjects [478]. This study reported elevated IDO1 expression in H. pylori-infected, but not uninfected, samples that inversely correlates with the severity of gastritis.…”

Section: Micro-organism Induction Of Ido1 In Vivosupporting

confidence: 46%

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Role of indoleamine 2,3-dioxygenase in health and disease

et al. 2015

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IDO1 (indoleamine 2,3-dioxygenase 1) is a member of a unique class of mammalian haem dioxygenases that catalyse the oxidative catabolism of the least-abundant essential amino acid, L-Trp (L-tryptophan), along the kynurenine pathway. Significant increases in knowledge have been recently gained with respect to understanding the fundamental biochemistry of IDO1 including its catalytic reaction mechanism, the scope of enzyme reactions it catalyses, the biochemical mechanisms controlling IDO1 expression and enzyme activity, and the discovery of enzyme inhibitors. Major advances in understanding the roles of IDO1 in physiology and disease have also been realised. IDO1 is recognised as a prominent immune regulatory enzyme capable of modulating immune cell activation status and phenotype via several molecular mechanisms including enzyme-dependent deprivation of L-Trp and its conversion into the aryl hydrocarbon receptor ligand kynurenine and other bioactive kynurenine pathway metabolites, or non-enzymatic cell signalling actions involving tyrosine phosphorylation of IDO1. Through these different modes of biochemical signalling, IDO1 regulates certain physiological functions (e.g. pregnancy) and modulates the pathogenesis and severity of diverse conditions including chronic inflammation, infectious disease, allergic and autoimmune disorders, transplantation, neuropathology and cancer. In the present review, we detail the current understanding of IDO1's catalytic actions and the biochemical mechanisms regulating IDO1 expression and activity. We also discuss the biological functions of IDO1 with a focus on the enzyme's immune-modulatory function, its medical implications in diverse pathological settings and its utility as a therapeutic target.

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Section: Micro-organism Induction Of Ido1 In Vivosupporting

confidence: 46%

“…Moreover, ex vivo inhibition of IDO1 in gastric biopsy cultures with 1-L-MT resulted in the increased expression of Th1-type markers of inflammation (i.e. IFNγ , Tbet and IL-17) and a reduced Th2 marker (IL-4), supporting an antiinflammatory action of IDO1 [478].…”

Section: Micro-organism Induction Of Ido1 In Vivomentioning

confidence: 79%

Role of indoleamine 2,3-dioxygenase in health and disease

et al. 2015

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“…This mechanism lowers gastric inflammation, possibly contributing to the persistence of HP. 24 Chen and Blaser 25 suggest that the intensity of the response of the host against especially aggressive HP strands (with the cagA gene) might alter the pattern of Th1/Th2 immune response with the subsequent induction of immunoregulating lymphocytes that may prevent immune hyper-reactivity responses, such as asthma or allergy in cases where the Th2 pattern is predominant. It is very well known that intensity of TBI and chemotherapy used during conditioning dictate the integrity of the gastrointestinal mucosa and the subsequent transfer of bacterial lipopolysaccharide and other 'danger/pathogen-associated molecular patterns' (DAMPS/PAMPS) into the systemic circulation.…”

Section: Discussionmentioning

confidence: 99%

Potential protective effect of Helicobacter pylori on the development of gastrointestinal GvHD

Velasco-Guardado

Mora-Soler

López-Corral

et al. 2016

Bone Marrow Transplant

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Previous reports ascribe a modulating capacity of the immune response to Helicobacter pylori (HP). Our hypothesis was to demonstrate in a prospective study that HP infection could have a protective effect against development of gastrointestinal GvHD in patients receiving allogeneic hematopoietic cell transplantation (HCT). Presence of HP before transplant was determined using C 13 urea breath test. Seventy-nine patients receiving an allogeneic HCT were included and 93.7% of them received PBSC; in 51.9%, the donor was unrelated. Acute gastrointestinal GvHD was diagnosed in 51.9% (n = 41). In the multivariable analysis, HP infection was associated with a lower frequency of gastrointestinal GvHD (odds ratio (OR) = 0.19 (95% confidence interval (CI): 0.05-0.67); in contrast, an unrelated donor was associated with a higher frequency of gastrointestinal GvHD (odds ratio = 5.4 (95% confidence interval: 1.6-18.2). One year overall survival (OS) was 74%. In the multivariate Cox proportional-hazards regression analysis, stages 0-II gastrointestinal GvHD (hazards ratio (HR) = 0.19), reduced intensity conditioning (HR = 0.04) and tacrolimus-sirolimus GvHD prophylaxis (HR = 0.06) were all associated with a better OS. In summary, HP infection could have a role in decreasing gastrointestinal GvHD in patients receiving allogeneic HCT from peripheral blood including related and unrelated donors.

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“…One such anti-inflammatory factor is indoleamine 2,3 dioxygenase (IDO) which depletes tryptophan (an essential amino acid for the host) in the environment. Larussa et al [16] report that IDO expression was enhanced in gastric biopsies from H. pylori infected compared with uninfected individuals. This would indicate that immune cells would be affected by the tryptophan deficiency, and indeed, the study also found that the levels of IDO expression correlated inversely with the gastritis score in H. pylori-infected gastric mucosa, but not in uninfected mucosa.…”

Section: Adaptive Immune Responses To H Pylori Infectionmentioning

confidence: 99%

Inflammation, Immunity, and Vaccines for Helicobacter pylori Infection

2015

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During the last year, a variety of studies have been published that increases our understanding of the basic mechanisms of immunity and inflammation in Helicobacter pylori infection and progression to gastric cancer. Innate immune regulation and epithelial cell response were covered by several studies that contribute with new insights in the host response to H. pylori infection. Also, the adaptive immune response to H. pylori and particularly the role of IL-22 have been addressed in some studies. These advances may improve vaccine development where new strategies have been published. Two major studies analyzed H. pylori genomes of 39 worldwide strains and looked at the protein profiles. In addition, multi-epitope vaccines for therapeutic use have been investigated. Studies on different adjuvants and delivery systems have also given us new insights. This review presents articles from the last year that reveal detailed insight into immunity and regulation of inflammation, the contribution of immune cells to the development of gastric cancer, and understanding mechanisms of vaccine-induced protection.Approximately 1 in 10 Helicobacter pylori-infected individuals will develop disease, including peptic ulcer disease, and in the worst case 1 in 100 will develop gastric cancer. Whether infection will lead to symptoms (or not) is dependent both on the host and bacterial genetics [1]. In infected individuals, activation of innate and adaptive immune system leads to the recruitment to the stomach of a wide range of inflammatory cell types, including dendritic cells, macrophages, neutrophils, mast cells, and T and B cells [2]. The recruited immune cells secrete a range of pro-inflammatory cytokines such as IL-1, TNF, IFNc, and IL-17 that lead to the chronic active inflammation that is characteristic of H. pylori infection.The highest prevalence of H. pylori disease is found in low-and middle-income countries where the infection is endemic. As the access to health care is improving in low-and middle-income countries, the positive effects on increasing life expectancy is predicted to be overshadowed by the increasing incidence of gastric cancer due to H. pylori infection [3]. Antibiotic treatment can cure peptic ulcer disease and reduce the lifetime risk of gastric cancer. However, reinfection is accompanied by the return of peptic ulcer disease and the risk of gastric cancer. Primary infection does not induce an immune response that protects against a second encounter with the bacteria. Given the difficulty in eradicating H. pylori infection, there is a need to develop novel strategies, ideally, a highly efficacious vaccine. The lack of natural immunity means that we will require a detailed understanding of the H. pylori bacteria and its interplay with the human host if vaccination and therapeutic approaches are to be successful.The studies published in the last year have increased our understanding of the interaction of the bacteria with the host and its effects on immune response and inflammation. In addition, vac...

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Enhanced Expression of Indoleamine 2,3‐Dioxygenase in Helicobacter pylori‐Infected Human Gastric Mucosa Modulates Th1/Th2 Pathway and Interleukin 17 Production

Cited by 27 publications

References 31 publications

Role of indoleamine 2,3-dioxygenase in health and disease

Role of indoleamine 2,3-dioxygenase in health and disease

Potential protective effect of Helicobacter pylori on the development of gastrointestinal GvHD

Inflammation, Immunity, and Vaccines for Helicobacter pylori Infection

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