Induction of nitric oxide synthesis in murine macrophages by Helicobacter pylori

Shapiro, Kenneth B.; Hotchkiss, Joseph H.

doi:10.1016/0304-3835(96)04154-7

Cited by 40 publications

(34 citation statements)

References 29 publications

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“…NO generation by macrophages is activated by intact bacteria or by soluble components of H. pylori and does not require the presence of H. pylori LPS (11,13). In addition, H. pylori medium filtrates cause macrophage NO synthesis (14), supporting the hypothesis that factors released from H. pylori are activators of iNOS.…”

mentioning

confidence: 60%

Cutting Edge: Urease Release by Helicobacter pylori Stimulates Macrophage Inducible Nitric Oxide Synthase

Gobert

Mersey

Cheng

et al. 2002

The Journal of Immunology

121

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Inducible NO synthase (iNOS) expression and production of NO are both up-regulated with Helicobacter pylori infection in vivo and in vitro. We determined whether major pathogenicity proteins released by H. pylori activate iNOS by coculturing macrophages with wild-type or mutant strains deficient in VacA, CagA, picB product, or urease (ureA−). When filters were used to separate H. pylori from macrophages, there was a selective and significant decrease in stimulated iNOS mRNA, protein, and NO2− production with the ureA− strain compared with wild-type and other mutants. Similarly, macrophage NO2− generation was increased by H. pylori protein water extracts of all strains except ureA−. Recombinant urease stimulated significant increases in macrophage iNOS expression and NO2− production. Taken together, these findings indicate a new role for the essential H. pylori survival factor, urease, implicating it in NO-dependent mucosal damage and carcinogenesis.

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mentioning

confidence: 60%

Cutting Edge: Urease Release by Helicobacter pylori Stimulates Macrophage Inducible Nitric Oxide Synthase

Gobert

Mersey

Cheng

et al. 2002

The Journal of Immunology

121

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“…Many studies have indicated that ROMs can directly interact with genomic DNA and cause damage in specific genes that control cell growth and differentiation [46][47][48] . Furthermore, it has been reported that intact H. pylori, as well as isolated cellular components, stimulate nitric oxide (NO) synthesis [49][50][51] . High concentrations of NO induce wild-type p53 protein accumulation [52,53] , and the NO-related deamination of DNA has been reported to cause GC-AT transitions, which are frequently found in p53 mutations in gastric cancer [23,54] .…”

Section: Oxidative Dna Damage and P53mentioning

confidence: 99%

Molecular mechanisms ofH. pyloriassociated gastric carcinogenesis

Zhang¹,

Farthing²

1999

WJG

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“…The absence of a relationship between H. pylori infection and nitrate body burden was more surprising. The presence of H. pylori antibodies is usually associated with the presence of H. pylori infection in the gastric mucosa (Newel and Stacey, 1992 ) and the production of endogenous nitrate by macrophages in a media infected by H. pylori has been demonstrated during in vitro experiments (Shapiro and Hotchkiss, 1996 ). Nevertheless, the amount formed during gastric inflammation may be too low to be detected with our study design.…”

Section: Discussionmentioning

confidence: 72%

“…Since endogenous nitrate formation could be important in certain specific conditions, namely diarrhea ( Wettig et al, 1991 ) , H. pylori infection (Shapiro and Hotchkiss, 1996 ), and possibly other inflammatory states (National Research Council, 1995 ), their effect was evaluated in the present study. Neither had any influence on urinary nitrate excretion, but few participants had diarrhea during the last 24 h ( n= 7 ) and no participant had an acute inflammatory state, as indicated by a concentration of C reactive protein in serum greater than 100 mg /l (Young et al, 1991 ) .…”

Section: Discussionmentioning

confidence: 99%

Sources of nitrate exposure in residents of rural areas in Quebec, Canada

Levallois

Ayotte

Louchini

et al. 2000

J Expo Sci Environ Epidemiol

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Nitrate exposure was investigated in a group of 187 people using well water and living in four areas of rural Quebec ( Canada ) with intensive agricultural activities. Nitrate intake was evaluated using a 24 -h dietary recall and a food frequency questionnaire, in conjunction with a validated food database and measurements of nitrate concentrations in private wells. The total internal dose was estimated by means of the 24 -h urinary nitrate excretion, while taking into account risk factors for endogenous nitrate formation. Mean ( geometric ) 24 -h urinary nitrate excretion was 16.9 mg N for the 100 people with low groundwater contamination ( mean nitrate concentration = 0.18 mg N / l ) and 23.3 mg N in the 87 individuals with moderate groundwater contamination ( mean nitrate concentration = 7.1 mg N / l ) . A multivariate analysis revealed that dietary nitrate intake during the last 24 h was the principal source of exposure, followed by water intake during the last 24 h. The Quetelet index was also a significant predictor of urinary excretion. The total predictive model explained only 29% of the variability in urinary nitrate excretion ( R 2 = 0.286 ) . Neither the inflammatory status as indicated by elevated C reactive protein, the presence of Helicobacter pylori antibodies nor the occurrence of diarrhea during the last 24 h prior to urine collection were associated with urinary nitrate excretion. In conclusion, food and to a lesser extent water contribute to nitrate exposure in this rural setting with moderate water contamination. Better predictors of endogenous nitrate production are needed to improve our ability to model nitrate body burden and estimate associated health risks.

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Induction of nitric oxide synthesis in murine macrophages by Helicobacter pylori

Cited by 40 publications

References 29 publications

Cutting Edge: Urease Release by Helicobacter pylori Stimulates Macrophage Inducible Nitric Oxide Synthase

Cutting Edge: Urease Release by Helicobacter pylori Stimulates Macrophage Inducible Nitric Oxide Synthase

Molecular mechanisms ofH. pyloriassociated gastric carcinogenesis

Sources of nitrate exposure in residents of rural areas in Quebec, Canada

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