ArticleInflammation2001
Hyperalgesia and edema responses induced by rat peripheral blood mononuclear cells incubated with carrageenin.
Article in Inflammation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed, 8 citations in OpenAlex.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to verify the role played by mononuclear cells in an acute (nonimmune) inflammatory reaction. Mononuclear cells purified from rat peripheral blood were incubated for 1, 2, or 24 h with 100 or 250 microg/ml carrageenin (Cg). The resultant donor supernatant was injected into recipient rats to test its ability to induce hyperalgesia (reduction in threshold for paw pressure) and edema (increase in paw volume). Mononuclear cell supernatants (MnS) induced a significant time- and dose-dependent hyperalgesia and edema in rat paws, which reached a maximal effect at 3 h, lasted for 6 h, and returned to basal levels at 24 h of injection. Prostaglandins and cytokines (interleukin 1, 2, 6, 8, and tumor necrosis factor alpha) accounted for the hyperalgesia induced by MnS, as it was reduced (40 to 90%) by synthesis inhibitors such as indomethacin, dexamethasone, rolipram, and cyclosporin added to the cultures at a microgram dose-range. Edema was dependent on serotonin release in rat paws. These results indicate that mononuclear cells may be important contributors to acute inflammatory reactions, especially under those conditions where pain is an important component.
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Registered trials
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