ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Disruption of nitric oxide signaling by Helicobacter pylori results in enhanced inflammation by inhibition of heme oxygenase-1.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.Archives of microbiology · 2026Review
- Plant-derived extracts or compounds for Helicobacter-associated gastritis: a systematic review of their anti-Helicobacter activity and anti-inflammatory effect in animal experiments.Chinese medicine · 2025Review
- Role ofWorld journal of gastroenterology · 2024Article
- Article
- BRD4 Regulates Glycolysis-Dependent Nos2 Expression in Macrophages Upon H pylori Infection.Cellular and molecular gastroenterology and hepatology · 2024Article
- The immunopathogenesis ofFrontiers in microbiology · 2024Review
- Helicobacter pylori-induced DNA double-stranded break in the development of gastric cancer.Cancer science · 2022Review
- Dietary intake of walnut preventedJournal of clinical biochemistry and nutrition · 2021Article
- MEK Inhibitor Reverses Metaplasia and Allows Re-Emergence of Normal Lineages in Helicobacter pylori-Infected Gerbils.Gastroenterology · 2019Article
- A Central Role for Heme Oxygenase-1 in the Control of Intestinal Epithelial Chemokine Expression.Journal of innate immunity · 2018Article
- Arginase 2 deletion leads to enhanced M1 macrophage activation and upregulated polyamine metabolism in response to Helicobacter pylori infection.Amino acids · 2016Article
- EGFR regulates macrophage activation and function in bacterial infection.The Journal of clinical investigation · 2016Article
- TRAP-positive osteoclast precursors mediate ROS/NO-dependent bactericidal activity via TLR4.Free radical biology & medicine · 2016Article
- Heme oxygenase-1 dysregulates macrophage polarization and the immune response to Helicobacter pylori.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- At the Bench: Helicobacter pylori, dysregulated host responses, DNA damage, and gastric cancer.Journal of leukocyte biology · 2014Review
- Role of the Helicobacter pylori-induced inflammatory response in the development of gastric cancer.Journal of cellular biochemistry · 2013Review
- Gastric cancer incidence and mortality is associated with altitude in the mountainous regions of Pacific Latin America.Cancer causes & control : CCC · 2013Article
- Haem oxygenase-1 inhibits phosphorylation of the Helicobacter pylori oncoprotein CagA in gastric epithelial cells.Cellular microbiology · 2013Article
- L-arginine uptake by cationic amino acid transporter 2 is essential for colonic epithelial cell restitution.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Chronic inflammation and oxidative stress: the smoking gun for Helicobacter pylori-induced gastric cancer?Gut microbesReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 3 countries.
Funding
Abstract
A strong cellular cross-talk exists between the pathogen Helicobacter pylori and high-output NO production. However, how NO and H. pylori interact to signal in gastric epithelial cells and modulate the innate immune response is unknown. We show that chemical or cellular sources of NO induce the anti-inflammatory effector heme oxygenase-1 (HO-1) in gastric epithelial cells through a pathway that requires NF-κB. However, H. pylori decreases NO-induced NF-κB activation, thereby inhibiting HO-1 expression. This inhibitory effect of H. pylori results from activation of the transcription factor heat shock factor-1 by the H. pylori virulence factor CagA and by the host signaling molecules ERK1/2 and JNK. Consistent with these findings, HO-1 is downregulated in gastric epithelial cells of patients infected with cagA(+) H. pylori but not in gastric epithelial cells of patients infected with cagA(-) H. pylori. Enhancement of HO-1 activity in infected cells or in H. pylori-infected mice inhibits chemokine generation and reduces inflammation. These data define a mechanism by which H. pylori favors its own pathogenesis by inhibiting HO-1 induction through the action of CagA.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.