Up‐Regulation of Inducible Nitric Oxide Synthase and Nitric Oxide in Helicobacter pylori‐Infected Human Gastric Epithelial Cells: Possible Role of Interferon‐γ in Polarized Nitric Oxide Secretion

Kim, Jung Mogg; Kim, Sang Woo; Jung, Hyun Chae; Song, In Sung; Kim, Chung Yong

doi:10.1046/j.1083-4389.2002.00068.x

Cited by 36 publications

(36 citation statements)

References 45 publications

(67 reference statements)

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“…However, other in vitro studies demonstrated that H. pylori infection and IFN-␥ act synergistically, for example, to induce apoptosis (29) and increase major histocompatibility complex class II (20) and iNOS (34) expression. One possible explanation for this discrepancy is that in other models IFN-␥ was introduced prior to or simultaneously with bacterial infection (20,34) rather than, as in this study, after a period of infection. Whether the effect of H. pylori infection on IFN-␥-dependent cell functions in vivo is synergistic or inhibitory ultimately may also depend on the balance between STAT1 and non-STAT1 IFN-␥ signaling (23,42) and on the influence of other cytokines, such as tumor necrosis factor alpha and IL-1␤, secreted by immune cells in the gastric mucosa (61).…”

Section: Discussionmentioning

confidence: 43%

Helicobacter pyloriDisrupts STAT1-Mediated Gamma Interferon-Induced Signal Transduction in Epithelial Cells

et al. 2004

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Section: Discussionmentioning

confidence: 43%

Helicobacter pyloriDisrupts STAT1-Mediated Gamma Interferon-Induced Signal Transduction in Epithelial Cells

et al. 2004

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“…sequestration and production of antibacterial peroxide species during the inflammatory response (36,37). Myeloperoxidase (MPO) and nitric oxide synthase 2 (NOS2) also limit bacterial growth by production of hypochlorous acid and NO, respectively (38)(39)(40). In a whole-genome microarray screen of duodenal biopsy specimens taken from cholera patients, genes for these four proteins consistently displayed the same regulatory patterns (2, 6).…”

Section: Discussionmentioning

confidence: 99%

Comparative Proteomic Analysis Reveals Activation of Mucosal Innate Immune Signaling Pathways during Cholera

et al. 2015

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i Vibrio cholerae O1 is a major cause of acute watery diarrhea in over 50 countries. Evidence suggests that V. cholerae O1 may activate inflammatory pathways, and a recent study of a Bangladeshi population showed that variants in innate immune genes play a role in mediating susceptibility to cholera. We analyzed human proteins present in the small intestine of patients infected with V. cholerae O1 to characterize the host response to this pathogen. We collected duodenal biopsy specimens from patients with acute cholera after stabilization and again 30 days after initial presentation. Peptides extracted from biopsy specimens were sequenced and quantified using label-free mass spectrometry and SEQUEST. Twenty-seven host proteins were differentially abundant between the acute and convalescent stages of infection; the majority of these have known roles in innate defense, cytokine production, and apoptosis. Immunostaining confirmed that two proteins, WARS and S100A8, were more abundant in lamina propria cells during the acute stage of cholera. Analysis of the differentially abundant proteins revealed the activation of key regulators of inflammation by the innate immune system, including Toll-like receptor 4, nuclear factor kappa-light-chain-enhancer of activated B cells, mitogen-activated protein kinases, and caspase-dependent inflammasomes. Interleukin-12␤ (IL-12␤) was a regulator of several proteins that were activated during cholera, and we confirmed that IL-12␤ was produced by lymphocytes recovered from duodenal biopsy specimens of cholera patients. Our study shows that a broad inflammatory response is generated in the gut early after onset of cholera, which may be critical in the development of long-term mucosal immunity against V. cholerae O1. Vibrio cholerae O1, which causes 3 to 5 million cases of cholera annually, is a noninvasive pathogen that does not penetrate the intestinal mucosa of human hosts (1, 2). Cholera is considered a prototypical, noninflammatory diarrheal illness, and there are no gross changes in the integrity of mucosal tissue during V. cholerae O1 infection (2, 3). However, there is mounting evidence that V. cholerae O1 triggers inflammatory responses in the gut (2, 4, 5). Studies of duodenal tissue extracted from cholera patients indicate that V. cholerae O1 infection causes upregulation of innate host defenses in the intestinal mucosa, including neutrophil-derived antibacterial proteins, proinflammatory cytokines, and BPIFB1 (also known as LPLUNC1), which is an immune-modifying defense protein that may attenuate the host response to bacterial lipopolysaccharide (LPS) (4-6). A candidate gene study showed that a variant in the promoter region of LPLUNC1 is associated with cholera susceptibility in a population in Bangladesh, an area where cholera is an ancient disease (7).Genome-wide association studies also underscore the importance of the innate immune system in influencing the clinical manifestations of V. cholerae O1 infection (8). A recent analysis of signals of natural selection in in...

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“…The Caco-2 cell line is a well-characterized model of the gut epithelium and is capable of differentiation and polarization (16), and it releases several inflammatory mediators upon treatment with H. pylori (23). It also provides a suitable and frequently cited method for studying the effects of infectious agents as well as probiotic bacteria (47).…”

Section: Fig 4 Effects Of Probiotics Andmentioning

confidence: 99%

Effects of Multispecies Probiotic Combination on Helicobacter pylori Infection In Vitro

Myllyluoma

Ahonen

Korpela

et al. 2008

Clin Vaccine Immunol

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Up‐Regulation of Inducible Nitric Oxide Synthase and Nitric Oxide in Helicobacter pylori‐Infected Human Gastric Epithelial Cells: Possible Role of Interferon‐γ in Polarized Nitric Oxide Secretion

Abstract: These results suggest that apical NO production mediated by MAP kinase in H. pylori-infected gastric epithelial cells may influence the bacteria and basolateral production of NO and IL-8 may play a role in the tissue inflammation.

Cited by 36 publications

References 45 publications

Helicobacter pyloriDisrupts STAT1-Mediated Gamma Interferon-Induced Signal Transduction in Epithelial Cells

Helicobacter pyloriDisrupts STAT1-Mediated Gamma Interferon-Induced Signal Transduction in Epithelial Cells

Comparative Proteomic Analysis Reveals Activation of Mucosal Innate Immune Signaling Pathways during Cholera

Effects of Multispecies Probiotic Combination on Helicobacter pylori Infection In Vitro

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