ArticleInflammation1992
Respiratory burst capacity of activated macrophages is resistant to depression by erythrocyte phagocytosis.
Article in Inflammation, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed, 7 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The present study evaluated whether macrophage activation would reduce the depression in the capacity of macrophages to produce H2O2 following EIgG phagocytosis. Macrophage activation was accomplished by exposing inflammatory rat peritoneal macrophages to 10 units of IFN gamma for 72 h. IFN gamma treatment caused a four to fivefold increase in phorbol myristate acetate (PMA)-triggered H2O2 production, but Fc receptor phagocytic function was unaltered. IFN gamma-activated macrophages were able to phagocytize a greater number of EIgG before a decrease in PMA-triggered H2O2 production was observed and the level of H2O2 production did not fall below that of untreated-inflammatory macrophages that had not received an EIgG phagocytic challenge. The depression in Fc receptor phagocytic function was unaltered with macrophage activation. These results indicate that activated macrophages are resistant to the depression of respiratory burst capacity caused by erythrocyte phagocytosis and suggests that IFN gamma treatment may be effective in preventing the impairment of host defense against bacterial infection that is associated with erythrocyte phagocytosis.
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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.