The immune Battle against helicobacter pylori infection: NO offense
Open accessAbstract
Helicobacter pylori is a successful pathogen of the human stomach. Despite a vigorous immune response by the gastric mucosa, the bacterium survives in its ecological niche, thus favoring diseases ranging from chronic gastritis to adenocarcinoma. The current literature demonstrates that high-output of nitric oxide (NO) production by the inducible enzyme NO synthase-2 (NOS2) plays major functions in host defense against bacterial infections. However, pathogens have elaborated several strategies to counteract the deleterious effects of NO; this includes inhibition of host NO synthesis and transcriptional regulation in response to reactive nitrogen species, allowing the bacteria to face the nitrosative stress. Moreover, NO is also a critical mediator of inflammation and carcinogenesis. In this context, we review the recent findings on the expression of NOS2 in H. pylori-infected gastric tissues and epithelial cells, the role of NO in H. pylori-related diseases and H. pylori gene expression, and the mechanisms whereby H. pylori regulates NO synthesis by host cells.
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Helicobacter pylori is linked to peptic ulcer disease, gastric cancer, as well as diabetes, autoimmune disease, chronic inflammation, CVD and endothelial dysfunction.
“Epidemiologically, H. pylori is linked to peptic ulcer disease, gastric cancer, as well as diabetes, autoimmune disease, chronic inflammation, CVD and endothelial dysfunction[240–245].”
From Enterosalivary nitrate metabolism and the microbiome: Intersection of microbial metabolism, nitric oxide and diet in cardiac and pulmonary vascular health (2017) · cites this paper as [242]
H. pylori has been shown to inhibit iNOS expression and NO production by the host macrophage.
“First, H. pylori has been shown to inhibit iNOS expression and NO production by the host macrophage[242].”
From Enterosalivary nitrate metabolism and the microbiome: Intersection of microbial metabolism, nitric oxide and diet in cardiac and pulmonary vascular health (2017) · cites this paper as [242]
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.
“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].”
From Enterosalivary nitrate metabolism and the microbiome: Intersection of microbial metabolism, nitric oxide and diet in cardiac and pulmonary vascular health (2017) · cites this paper as [242]
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- Authors
- Gobert, A. P., & Wilson, K. T.
- Affiliations
- Vanderbilt University Medical Center (US)
- VA Tennessee Valley Healthcare System (US)
- Corresponding author
- Wilson, Keith T.
- Venue
- Trends in Microbiology
- Publisher
- Elsevier BV
- Published
- 2016-05
- Volume
- 24
- Issue
- 5
- Pages
- 366-376
- ISSN
- 0966-842X (ISSN-L)
- PMC
- PMC4841705
- OpenAlex
- W2274755917
- Cited by
- 63
- References
- 84
- Citations by year
- 2026: 6 · 2025: 2 · 2024: 5 · 2023: 7 · 2022: 6 · 2021: 8 · 2020: 3 · 2019: 6 · 2018: 4 · 2017: 12 · 2016: 4
- FWCI
- 1.72
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Microbiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01 BX001453)
- National Institutes of Health
- National Cancer Institute (P01CA028842, R01CA190612, P01CA116087)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK053620, P30DK058404)
- National Center for Complementary and Integrative Health (R01AT004821)
- Topics
- Health Sciences › Medicine › Surgery › Helicobacter pylori-related gastroenterology studies
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- Helicobacter pylori, nitric oxide, host defense, nitrosative stress, gastric mucosa, chronic gastritis, gastric adenocarcinoma, inflammation, carcinogenesis, bacterial gene regulation, reactive nitrogen species
- MeSH terms
- Animals, Chronic Disease, Gastric Mucosa, Gastritis, Humans, Nitric Oxide, Stomach Neoplasms, Helicobacter pylori, Helicobacter Infections, Nitric Oxide Synthase Type II, Host-Pathogen Interactions
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