Helicobacter pylori induces IL-1β and IL-18 production in human monocytic cell line through activation of NLRP3 inflammasome via ROS signaling pathway

Li, Xiang; Liu, Sheng; Luo, Jingjing; Liu, Anyuan; Tang, Shuangyang; Liu, Shuo; Yu, Min; Zhang, Yan

doi:10.1093/femspd/ftu024

Cited by 58 publications

(44 citation statements)

References 44 publications

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“…This effect was observed in the early events post-infection [115], suggesting that the oxidative burst, rather than the effect of SMOX is involved. These results are also consistent with in vitro data showing that the partial scavenging of ROS by N-acetylcysteine led to a decrease of H. pylori -induced inflammasome formation and production of IL-1β and IL-18 by the human monocytic cell line THP-1 [116]. …”

Section: Endogenous Effect Of Ros On the Hostsupporting

confidence: 91%

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: Endogenous Effect Of Ros On the Hostsupporting

confidence: 91%

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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“…In contrast, a second study reported that gp91 phox−/− mice exhibit more inflammation and increased monoculear cell infiltration in the mucosa during infection with H. felis or H. pylori (Blanchard et al 2003). Although this investigation was performed at 3-weeks post-infection, which is not sufficient time to observe strong gastric inflammation, the results are consistent with in vitro data showing that the partial scavenging of ROS by N-acetylcysteine led to a decrease of H. pylori -induced inflammasome formation, and IL-1β and IL-18 production by H. pylori -infected THP-1 cells (Li et al 2015). …”

Section: Induction and Role Of Rossupporting

confidence: 86%

Human and Helicobacter pylori Interactions Determine the Outcome of Gastric Diseases

Gobert

Wilson

2017

Current Topics in Microbiology and Immunology

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The innate immune response is a critical hallmark of Helicobacter pylori infection. Epithelial and myeloid cells produce effectors, including the chemokine CXCL8, reactive oxygen species (ROS), and nitric oxide (NO), in response to bacterial components. Mechanistic and epidemiologic studies have emphasized that dysregulated and persistent release of these products leads to the development of chronic inflammation and to the molecular and cellular events related to carcinogenesis. Moreover, investigations in H. pylori-infected patients about polymorphisms of the genes encoding CXCL8 and inducible NO synthase, and epigenetic control of the ROS-producing enzyme spermine oxidase, have further proven that overproduction of these molecules impacts the severity of gastric diseases. Lastly, the critical effect of the crosstalk between the human host and the infecting bacterium in determining the severity of H. pylori-related diseases has been supported by phylogenetic analysis of the human population and their H. pylori isolates in geographic areas with varying clinical and pathologic outcomes of the infection.

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“…Indeed, recent several studies reported the signaling pathways for IL-1β production (16,19,29). However, the detailed mechanism of H. pylori-mediated IL-1β induction remains fully clarified.…”

Section: Quantitative-rt-pcrmentioning

confidence: 99%

Helicobacter pylori induces IL-1β protein through the inflammasome activation in differentiated macrophagic cells

et al. 2016

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More than 50% of people in the world are infected with Helicobacter pylori (H. pylori), which induces various gastric diseases. Especially, epidemiological studies have shown that H. pylori infection is a major risk factor for gastric cancer. It has been reported that the levels of interleukin (IL)-1β are upregulated in gastric tissues of patients with H. pylori infection. In this study, we investigated the induction mechanism of IL-1β during H. pylori infection. We found that IL-1β mRNA and protein were induced in phorbol-12-myristate-13-acetate (PMA)-differentiated THP-1 cells after H. pylori infection. This IL-1β production was inhibited by a caspase-1 inhibitor and a ROS inhibitor. Furthermore, K + efflux and Ca 2+ signaling were also involved in this process. These data suggest that NOD-like receptor (NLR) family, pyrin domain containing 3 (NLRP3) and its complex, known as NLRP3 inflammasome, are involved in IL-1β production during H. pylori infection because it is reported that NLRP3 inflammasome is activated by ROS, K + efflux and/or Ca 2+ signaling. These findings may provide therapeutic strategy for the control of gastric cancer in H. pylori-infected patients.

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Helicobacter pylori induces IL-1β and IL-18 production in human monocytic cell line through activation of NLRP3 inflammasome via ROS signaling pathway

Cited by 58 publications

References 44 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

Human and Helicobacter pylori Interactions Determine the Outcome of Gastric Diseases

<i><b>Helicobacter pylori</b></i><b> induces IL-1β protein through the inflammasome activation in differentiated macrophagic </b><b>cells </b>

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