ArticleInfection and immunity1994
Tumor necrosis factor alpha augments nitric oxide-dependent macrophage cytotoxicity against Entamoeba histolytica by enhanced expression of the nitric oxide synthase gene.
Article in Infection and immunity, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 95 citations in OpenAlex.
- The macrophage polarization inFrontiers in immunology · 2024Article
- Regulatory Functions of Hypoxia in Host-Parasite Interactions: A Focus on Enteric, Tissue, and Blood Protozoa.Microorganisms · 2023Review
- Entamoeba histolytica activation of caspase-1 degrades cullin that attenuates NF-κB dependent signaling from macrophages.PLoS pathogens · 2021Article
- Heme oxygenase-1 inhibition promotes IFNγ- and NOS2-mediated control of Mycobacterium tuberculosis infection.Mucosal immunology · 2021Article
- The NF-κB Pathway: Modulation byFrontiers in cellular and infection microbiology · 2021Review
- Entamoeba histolytica stimulates the alarmin molecule HMGB1 from macrophages to amplify innate host defenses.Mucosal immunology · 2020Article
- Review
- Plasma membrane damage repair is mediated by an acid sphingomyelinase in Entamoeba histolytica.PLoS pathogens · 2019Article
- The macrophage cytoskeleton acts as a contact sensor upon interaction with Entamoeba histolytica to trigger IL-1β secretion.PLoS pathogens · 2017Article
- Septic cardiomyopathy: evidence for a reduced force-generating capacity of human atrial myocardium in acute infective endocarditis.Innovative surgical sciences · 2017Article
- The effect of IFN-γ and TGF-β in the functional activity of mononuclear cells in the presence of Entamoeba histolytica.Parasites & vectors · 2015Article
- Immune Evasion Mechanisms of Entamoeba histolytica: Progression to Disease.Frontiers in microbiology · 2015Review
- Peroxynitrite and peroxiredoxin in the pathogenesis of experimental amebic liver abscess.BioMed research international · 2014Review
- Differentiated control of deranged nitric oxide metabolism: a therapeutic option in sepsis?Critical care (London, England) · 2013Review
- Host immune response to intestinal amebiasis.PLoS pathogens · 2013Review
- CD4+ and CD8+ T cell- and IL-17-mediated protection against Entamoeba histolytica induced by a recombinant vaccine.Vaccine · 2011Article
- Association between TNF-alpha and Entamoeba histolytica diarrhea.The American journal of tropical medicine and hygiene · 2010Article
- Protection against intestinal amebiasis by a recombinant vaccine is transferable by T cells and mediated by gamma interferon.Infection and immunity · 2009Article
- Crosstalk at the initial encounter: interplay between host defense and ameba survival strategies.Current opinion in immunology · 2007Review
- L-arginine and cationic amino acid transporter 2B regulate growth and survival of Leishmania amazonensis amastigotes in macrophages.Infection and immunity · 2007Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO measured as nitrite, NO2-) is the major effector molecule produced by activated macrophages for in vitro cytotoxicity against Entamoeba histolytica trophozoites. In this study, we determine whether tumor necrosis factor alpha (TNF-alpha) produced by activated bone marrow-derived macrophages (BMM) is involved in the induction of the inducible NO synthase gene (mac-NOS) for NO-dependent amebicidal activity. TNF-alpha alone did not directly induce macrophage NO2- production to kill amebae; however, in combination with increasing concentrations of TNF-alpha and gamma interferon (IFN-gamma), BMM amebicidal activity and NO2- production progressively increased and showed a significant linear correlation. Antiserum to TNF-alpha and the NO synthase inhibitor NG-monomethyl L-arginine (L-NMMA) inhibited the synergistic effects of TNF-alpha and IFN-gamma. BMM activated with increasing concentrations of lipopolysaccharide (LPS) and IFN-gamma showed a significant linear correlation between TNF-alpha release and NO2- production. Antiserum to TNF-alpha suppressed TNF-alpha release, NO2- production, and amebicidal activity by 93, 53, and 86%, respectively. L-NMMA diminished NO2- production by 74% and macrophage amebicidal activity by 83% but had no effect on TNF-alpha release. Quantification by Northern (RNA) blot analyses demonstrated that IFN-gamma in combination with TNF-alpha or LPS increased markedly the accumulation of mac-NOS and TNF-alpha mRNAs in a time-dependent manner with a concomitant increase in NO and TNF-alpha production. Peak induction of mac-NOS occurred after 24 h, whereas TNF-alpha mRNA was rapidly expressed after 4 h and remained stable for 48 h. Taken together, these data argue that TNF-alpha augments NO-dependent macrophage cytotoxicity against E. histolytica via elevated levels of mac-NOS mRNA expression which may be associated with the accumulation of TNF-alpha mRNA.
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Registered trials
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.