+ Site Statistics
References:
54,258,434
Abstracts:
29,560,870
PMIDs:
28,072,757
+ Search Articles
+ PDF Full Text Service
How our service works
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ Translate
+ Recently Requested

Up-regulation of inducible nitric oxide synthase and nitric oxide in Helicobacter pylori-infected human gastric epithelial cells: possible role of interferon-gamma in polarized nitric oxide secretion



Up-regulation of inducible nitric oxide synthase and nitric oxide in Helicobacter pylori-infected human gastric epithelial cells: possible role of interferon-gamma in polarized nitric oxide secretion



Helicobacter 7(2): 116-128



Nitric oxide (NO) generated by nitric oxide synthase (NOS) is known to be an important modulator of the mucosal inflammatory response. In this study, we questioned whether Helicobacter pylori infection could up-regulate the epithelial cell inducible NOS (iNOS) gene expression and whether NO production could show polarity that can be regulated by immune mediators. Human gastric epithelial cell lines were infected with H. pylori, and the iNOS mRNA expression was assessed by quantitative RT-PCR. NO production was assayed by determining nitrite/nitrate levels in culture supernatants. To determine the polarity of NO secretion by the H. pylori-infected epithelial cells, Caco-2 cells were cultured as polarized monolayers in transwell chambers, and NO production was measured. iNOS mRNA levels were significantly up-regulated in the cells infected with H. pylori, and expression of iNOS protein was confirmed by Western blot analysis. Increased NO production in the gastric epithelial cells was seen as early as 18 hours postinfection, and reached maximal levels by 24 hours postinfection. The specific MAP kinase inhibitors decreased H. pylori-induced iNOS and NO up-regulation. After H. pylori infection of polarized epithelial cells, NO was released predominantly into the apical compartment, and IL-8 was released predominantly into basolateral compartment. The addition of IFN-gamma to H. pylori-infected polarized epithelial cells showed a synergistically higher apical and basolateral NO release. 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.

Please choose payment method:






(PDF emailed within 1 workday: $29.90)

Accession: 060445044

Download citation: RISBibTeXText

PMID: 11966872


Related references

Upregulation of inducible nitric oxide synthase and nitric oxide in Helicobacter pylori-infected human gastric epithelial cells Possible role of interferon-gamma in polarized nitric oxide secretion. Abstracts of the General Meeting of the American Society for Microbiology 101: 311-312, 2001

Up-regulation of inducible nitric oxide synthase and polarized nitric oxide secretion in Helicobacter pylori-infected human gastric epithelial cells Possible involvement of MAP kinase signaling pathway. Gastroenterology 120(5 Suppl. 1): A 659, 2001

Nitric oxide and inducible nitric oxide synthase are produced after Helicobacter pylori infection of cultured epithelial cells in vitro. Gastroenterology 114(4 Part 2): A986, April 15, 1998

Role of nitric oxide derived from inducible nitric oxide synthase in H. pylori-infected gastric mucosal injury. Nihon Rinsho. Japanese Journal of Clinical Medicine 63(Suppl. 11): 109-115, 2005

Inducible nitric oxide synthase and nitric oxide production in Leishmania infantum-infected human macrophages stimulated with interferon-gamma and bacterial lipopolysaccharide. International Journal of Clinical and Laboratory Research 29(3): 122-127, 1999

Expression of inducible nitric oxide synthase and nitric oxide-modified proteins in Helicobacter pylori-associated atrophic gastric mucosa. Journal of Gastroenterology and Hepatology 23(Suppl. 2): S250-S257, 2009

Role of inducible nitric oxide synthase-derived nitric oxide in lipopolysaccharide plus interferon-gamma-induced pulmonary inflammation. Toxicology and Applied Pharmacology 195(1): 45-54, 2004

Estrogen up-regulates inducible nitric oxide synthase, nitric oxide, and cyclooxygenase-2 in splenocytes activated with T cell stimulants: role of interferon-gamma. Endocrinology 147(2): 662-671, 2005

Defective nitric oxide effector functions lead to extreme susceptibility of Trypanosoma cruzi-infected mice deficient in gamma interferon receptor or inducible nitric oxide synthase. Infection and Immunity 66(3): 1208-1215, 1998

Regulation of nitric oxide production in cultured human T84 intestinal epithelial cells by nuclear factor-kappaB-dependent induction of inducible nitric oxide synthase after exposure to bacterial endotoxin. Alimentary Pharmacology & Therapeutics 14(7): 945-954, 2000

Helicobacter pylori infection of human gastric epithelial cells upregulates iNOS expression and induces the polarized secretion of nitric oxide. Gastroenterology 118(4 Suppl 2 Part 2): AGA A1256, 2000

C6 glioma cell insoluble matrix components enhance interferon-gamma-stimulated inducible nitric-oxide synthase/nitric oxide production in BV2 microglial cells. Journal of Biological Chemistry 283(5): 2526-2533, 2007

Endothelial nitric oxide synthase plays a main role in producing nitric oxide in the superacute phase of hepatic ischemia prior to the upregulation of inducible nitric oxide synthase. Journal of Surgical Research 183(2): 742-751, 2013

Inhibition by 1'-acetoxychavicol acetate of lipopolysaccharide- and interferon-gamma-induced nitric oxide production through suppression of inducible nitric oxide synthase gene expression in RAW264 cells. Carcinogenesis 19(6): 1007-1012, 1998

Beta-carotene inhibits Helicobacter pylori-induced expression of inducible nitric oxide synthase and cyclooxygenase-2 in human gastric epithelial AGS cells. Journal of Physiology and Pharmacology 60(Suppl. 7): 131-137, 2010