The Immune Battle against Helicobacter pylori Infection: NO Offense

Gobert, Alain P.; Wilson, Keith T.

doi:10.1016/j.tim.2016.02.005

Cited by 53 publications

(36 citation statements)

References 84 publications

(130 reference statements)

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“…The current knowledge about the resistance of H. pylori to the effectors of the innate immune response has evidenced one intriguing feature: the bacterium fights the nitrosative stress and also inhibits NO production by the host [35]; however, it appears to only inhibit ROS-dependent oxidative damage without attenuating the expression/activity of SMOX or NOX. This could be explained by the fact that the most reactive nitrogen species result from the reaction of NO and ROS (e.g.…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, ARG2 is also a natural competitor for inducible nitric oxide synthase (NOS2), the enzyme that generates nitric oxide (NO) from L-arginine. NO is a free radical produced by H. pylori -infected macrophages that exhibits anti-microbial properties and can regulate inflammation and carcinogenesis [35]. In H. pylori -infected macrophages, blocking ARG2 activity results in increased NO production [32], highlighting that the induction of the arginase metabolic pathway by the bacterium is one way of controlling NO production.…”

Section: Polyamine-dependent Ros Synthesis During H Pylori Infectionmentioning

confidence: 99%

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Polyamine- and NADPH-dependent generation of ROS during Helicobacter pylori infection: A blessing in disguise

Gobert

Wilson

2017

Free Radical Biology and Medicine

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Helicobacter pylori is a Gram-negative bacterium that specifically colonizes the gastric ecological niche. During the infectious process, which results in diseases ranging from chronic gastritis to gastric cancer, the host response is characterized by the activation of the innate immunity of gastric epithelial cells and macrophages. These cells thus produce effector molecules such as reactive oxygen species (ROS) to counteract the infection. The generation of ROS in response to H. pylori involves two canonical pathways: 1) the NADPH-dependent reduction of molecular oxygen to generate O2•−, which can dismute to generate ROS; and 2) the back-conversion of the polyamine spermine into spermidine through the enzyme spermine oxidase, leading to H2O2 production. Although these products have the potential to affect the survival of bacteria, H. pylori has acquired numerous strategies to counteract their deleterious effects. Nonetheless, ROS-mediated oxidative DNA damage and mutations may participate in the adaptation of H. pylori to its ecological niche. Lastly, ROS have been shown to play a major role in the development of the inflammation and carcinogenesis. It is the purpose of this review to summarize the literature about the production of ROS during H. pylori infection and their role in this infectious gastric disease.

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Section: Discussionmentioning

confidence: 99%

Section: Polyamine-dependent Ros Synthesis During H Pylori Infectionmentioning

confidence: 99%

Polyamine- and NADPH-dependent generation of ROS during Helicobacter pylori infection: A blessing in disguise

Gobert

Wilson

2017

Free Radical Biology and Medicine

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“…To survive the hostile gastric milieu, H. pylori has developed robust mechanisms for altering its local environment on two fronts. First, H. pylori has been shown to inhibit iNOS expression and NO production by the host macrophage[242]. Second, H. pylori can alter stomach pH via expression of urease that allows for the formation of both ammonia and bicarbonate from urea, thus reducing the acidity of the stomach and potentially reducing the nascent pH-dependent formation of NO from salivary nitrite[242,246,247].…”

Section: The Oral Microbiome and Bacterial Nitrate Reductionmentioning

confidence: 99%

Enterosalivary nitrate metabolism and the microbiome: Intersection of microbial metabolism, nitric oxide and diet in cardiac and pulmonary vascular health

Koch

Gladwin

Freeman

et al. 2017

Free Radical Biology and Medicine

132

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Recent insights into the bioactivation and signaling actions of inorganic, dietary nitrate and nitrite now suggest a critical role for the microbiome in the development of cardiac and pulmonary vascular diseases. Once thought to be the inert, end-products of endothelial-derived nitric oxide (NO) heme-oxidation, nitrate and nitrite are now considered major sources of exogenous NO that exhibit enhanced vasoactive signaling activity under conditions of hypoxia and stress. The bioavailability of nitrate and nitrite depend on the enzymatic reduction of nitrate to nitrite by a unique set of bacterial nitrate reductase enzymes possessed by specific bacterial populations in the mammalian mouth and gut. The pathogenesis of pulmonary hypertension (PH), obesity, hypertension and CVD are linked to defects in NO signaling, suggesting a role for commensal oral bacteria to shape the development of PH through the formation of nitrite, NO and other bioactive nitrogen oxides. Oral supplementation with inorganic nitrate or nitrate-containing foods exert pleiotropic, beneficial vascular effects in the setting of inflammation, endothelial dysfunction, ischemia-reperfusion injury and in pre-clinical models of PH, while traditional high-nitrate dietary patterns are associated with beneficial outcomes in hypertension, obesity and CVD. These observations highlight the potential of the microbiome in the development of novel nitrate- and nitrite-based therapeutics for PH, CVD and their risk factors.

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“…By contrast, pathological immunological niches are sites of tissue pathology where high levels of immune activity are associated with inflammation and tissue dysfunction. Examples of pathological immunological niches include tumours and inflamed, infected or ischaemic tissues 4–8 (FIG. 2).…”

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confidence: 99%

Regulation of immunity and inflammation by hypoxia in immunological niches

2017

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Immunological niches are focal sites of immune activity that can have varying microenvironmental features. Hypoxia is a feature of physiological and pathological immunological niches. The impact of hypoxia on immunity and inflammation can vary depending on the microenvironment and immune processes occurring in a given niche. In physiological immunological niches, such as the bone marrow, lymphoid tissue, placenta and intestinal mucosa, physiological hypoxia controls innate and adaptive immunity by modulating immune cell proliferation, development and effector function, largely via transcriptional changes driven by hypoxia-inducible factor (HIF). By contrast, in pathological immunological niches, such as tumours and chronically inflamed, infected or ischaemic tissues, pathological hypoxia can drive tissue dysfunction and disease development through immune cell dysregulation. Here, we differentiate between the effects of physiological and pathological hypoxia on immune cells and the consequences for immunity and inflammation in different immunological niches. Furthermore, we discuss the possibility of targeting hypoxia-sensitive pathways in immune cells for the treatment of inflammatory disease.

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The Immune Battle against Helicobacter pylori Infection: NO Offense

Cited by 53 publications

References 84 publications

Polyamine- and NADPH-dependent generation of ROS during Helicobacter pylori infection: A blessing in disguise

Polyamine- and NADPH-dependent generation of ROS during Helicobacter pylori infection: A blessing in disguise

Enterosalivary nitrate metabolism and the microbiome: Intersection of microbial metabolism, nitric oxide and diet in cardiac and pulmonary vascular health

Regulation of immunity and inflammation by hypoxia in immunological niches

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