ArticleInflammation1995
Blood polymorphonuclear leukocyte migratory activities during rheumatoid arthritis.
Article in Inflammation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed, 11 citations in OpenAlex.
- Blood polymorphonuclear leukocyte migration as a predictive marker for infections in severe trauma: comparison with various inflammation parameters.Intensive care medicine · 2004Article
- Blood polymorphonuclear leukocyte activation in atherosclerosis: effects of aspirin.Inflammation · 2001Article
- Peripheral blood neutrophil leukotriene B4 release and migration in rheumatoid arthritis.Inflammation · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Blood polymorphonuclear leukocyte (PMN) migratory activity was investigated in adult rheumatoid arthritis (RA) patients and in healthy control subjects using fresh whole blood in a novel membrane filter assay. The PMNs migrated under FMLP stimulation and under blank control conditions (spontaneous migration). Essential evaluation criteria were the percentage of PMNs that migrated from the entire blood sample into the filters (TMI) and the penetration depth of the migrating cell bulk into the filters (DC). PMNs from healthy subjects penetrate deeper under FMLP stimulation than under blank control conditions. Migration depends on age and sex: the TMI decreases, while the DC and the reactivity towards FMLP increase with age. FMLP triggers a stronger DC reaction in females than in males. Compared with healthy subjects, patients with RA develop an increased PMN reaction, whereas FMLP inhibits migration in comparison with the blank controls. There is no correlation between disease activity estimated by joint functions and PMN migratory activity, while there are strong correlations between disease activity and the classical RA laboratory parameters WBC, platelets, BSR, CRP, hemoglobin and rheumatoid factor. PMNs therefore probably do not play a major role in joint injury. Gold therapy inhibits DC reactivity. PMN migration in RA differs markedly from the reactions in juvenile rheumatoid arthritis, where high disease activity is associated with high PMN migratory activity, and the correlations between classical laboratory parameters and disease activity follow other patterns than in RA.
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