ArticleProceedings of the National Academy of Sciences of the United States of America2002
The quantity of nitric oxide released by macrophages regulates Chlamydia-induced disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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Who cites it
23 citing papers in PubMed, 64 citations in OpenAlex.
- Intestinal immune responses to commensal and pathogenic protozoa.Frontiers in immunology · 2022Review
- Review
- Infection-Induced Intestinal Dysbiosis Is Mediated by Macrophage Activation and Nitrate Production.mBio · 2019Article
- Mice Housed at Elevated Vivarium Temperatures Display Enhanced T-cell Response and Survival toComparative medicine · 2017Article
- Chlamydia muridarum infection of macrophages elicits bactericidal nitric oxide production via reactive oxygen species and cathepsin B.Infection and immunity · 2015Article
- Spermine oxidase is a regulator of macrophage host response to Helicobacter pylori: enhancement of antimicrobial nitric oxide generation by depletion of spermine.Amino acids · 2014Article
- Arginine and polyamines in Helicobacter pylori-induced immune dysregulation and gastric carcinogenesis.Amino acids · 2012Article
- IL-17A synergizes with IFN-γ to upregulate iNOS and NO production and inhibit chlamydial growth.PloS one · 2012Article
- Distinct roles for nitric oxide in resistant C57BL/6 and susceptible BALB/c mice to control Burkholderia pseudomallei infection.BMC immunology · 2011Article
- Immune evasion by Helicobacter pylori is mediated by induction of macrophage arginase II.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Exacerbation of chronic inflammatory diseases by infectious agents: Fact or fiction?World journal of diabetes · 2010Article
- Arginase II restricts host defense to Helicobacter pylori by attenuating inducible nitric oxide synthase translation in macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Article
- Temporal delay of peak T-cell immunity determines Chlamydia pneumoniae pulmonary disease in mice.Infection and immunity · 2008Article
- Genetic control of susceptibility to pulmonary infection with Chlamydia pneumoniae in the mouse.Genes and immunity · 2008Article
- Characterization of an acid-dependent arginine decarboxylase enzyme from Chlamydophila pneumoniae.Journal of bacteriology · 2007Article
- Role of inducible nitric oxide synthase and NADPH oxidase in early control of Burkholderia pseudomallei infection in mice.Infection and immunity · 2006Article
- Expression of matrix metalloproteinases subsequent to urogenital Chlamydia muridarum infection of mice.Infection and immunity · 2005Article
- Intranasal vaccination induces protective immunity against intranasal infection with virulent Francisella tularensis biovar A.Infection and immunity · 2005Article
- High prevalence of natural Chlamydophila species infection in calves.Journal of clinical microbiology · 2004Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Intracellular bacteria of the genus Chlamydia cause numerous typically chronic diseases, frequently with debilitating sequelae. Genetic determinants of disease susceptibility after infection with Chlamydia bacteria are unknown. C57BL/6 mice develop severe pneumonia and poor immunity against Chlamydia after moderate respiratory infection whereas BALB/c mice are protected from disease and develop vigorous Th1 immunity. Here we show that infected C57BL/6 macrophages release more NO synthesized by NO synthase 2 (NOS2) than BALB/c macrophages and have lower mRNA concentrations of arginase II, a competitor of NOS2 for the common substrate, l-arginine. Reduction, but not elimination, of NO production by incomplete inhibition of NOS2 abolishes susceptibility of C57BL/6 mice to Chlamydia-induced disease. Thus, the quantity of NO released by infected macrophages is the effector mechanism that regulates between pathogenic and protective responses to chlamydial infection, and genes controlling NO production determine susceptibility to chlamydial disease.
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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.