The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Helicobacter pylori arginase inhibits nitric oxide production by eukaryotic cells: A strategy for bacterial survival
Open accessAbstract
The antimicrobial effect of nitric oxide (NO) is an essential part of innate immunity. The vigorous host response to the human gastric pathogen Helicobacter pylori fails to eradicate the organism, despite up-regulation of inducible NO synthase (iNOS) in the gastric mucosa. Here we report that wild-type strains of H. pylori inhibit NO production by activated macrophages at physiologic concentrations of l-arginine, the common substrate for iNOS and arginase. Inactivation of the gene rocF, encoding constitutively expressed arginase in H. pylori, restored high-output NO production by macrophages. By using HPLC analysis, we show that l-arginine is effectively consumed in the culture medium by wild-type but not arginase-deficient H. pylori. The substantially higher levels of NO generated by macrophages cocultured with rocF-deficient H. pylori resulted in efficient killing of the bacteria, whereas wild-type H. pylori exhibited no loss of survival under these conditions. Killing of the arginase-deficient H. pylori was NO-dependent, because peritoneal macrophages from iNOS−/−mice failed to affect the survival of the rocF mutant. Thus, bacterial arginase allows H. pylori to evade the immune response by down-regulating eukaryotic NO production.
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Cites
The complete genome sequence of the gastric pathogen Helicobacter pylori
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Biochemistry of nitric oxide and its redox-activated forms
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Helicobacter pylori is killed by nitrite under acidic conditions
Dykhuizen, R. S., Fraser, A., McKenzie, H., Golden, M., Leifert, C., & Benjamin, N. (1998) · Gut · doi:10.1136/gut.42.3.334 · Cited by 131
The urea cycle of Helicobacter pylori
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Self-citation
Cited by
Pathogenesis of Helicobacter pylori Infection
Kusters, J. G., van Vliet, A. H. M., & Kuipers, E. J. (2006) · Clinical Microbiology Reviews · doi:10.1128/cmr.00054-05 · Cited by 2,526
Metabolic reprogramming in macrophages and dendritic cells in innate immunity
Kelly, B., & O'Neill, L. A. (2015) · Cell Research · doi:10.1038/cr.2015.68 · Cited by 1,876
Regulation of immune responses by L-arginine metabolism
Bronte, V., & Zanovello, P. (2005) · Nature Reviews Immunology · doi:10.1038/nri1668 · Cited by 1,775
Arginine metabolism and nutrition in growth, health and disease
Wu, G., Bazer, F. W., Davis, T. A., Kim, S. W., Li, P., Marc Rhoads, J., Carey Satterfield, M., Smith, S. B., Spencer, T. E., & Yin, Y. (2009) · Amino Acids · doi:10.1007/s00726-008-0210-y · Cited by 1,362
El Kasmi, K. C., Qualls, J. E., Pesce, J. T., Smith, A. M., Thompson, R. W., Henao-Tamayo, M., Basaraba, R. J., König, T., Schleicher, U., Koo, M.-S., et al. (2008) · Nature Immunology · doi:10.1038/ni.1671 · Cited by 646
Metadata
- Authors
- Gobert, A. P., McGee, D. J., Akhtar, M., Mendz, G. L., Newton, J. C., Cheng, Y., Mobley, H. L. T., & Wilson, K. T.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2001-11-20
- Volume
- 98
- Issue
- 24
- Pages
- 13844-13849
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2172260976
- Cited by
- 380
- References
- 6
- FWCI
- 14.59
- Type
- journal article
- Language
- en
- Open access
- green
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- Gobert, A. P., McGee, D. J., Akhtar, M., Mendz, G. L., Newton, J. C., Cheng, Y., Mobley, H. L. T., & Wilson, K. T. (2001). Helicobacter pylori arginase inhibits nitric oxide production by eukaryotic cells: A strategy for bacterial survival. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.241443798
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.