Docteur Romuald CHAMPY

Bibliographie

• COVID-19 outcomes in patients with inflammatory rheumatic and musculoskeletal diseases treated with rituximab: a cohort study

  2021

  ArticleThe Lancet Rheumatology

• Severity of COVID-19 and survival in patients with rheumatic and inflammatory diseases: data from the French RMD COVID-19 cohort of 694 patients

  2020

  ArticleAnnals of the Rheumatic Diseases

• Blood and Synovial Distribution of Angiogenin in Rheumatic Diseases

  1993

  ArticleArthritis and Rheumatism

Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).

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Top publications · les plus citées

• 1

  Reactive oxygen species and superoxide dismutases: role in joint diseases

  Joint bone spine · 2007

  📚 428 citations🎯 RCR 12.49Top 2% NIH
• 2

  Monosodium urate monohydrate crystal-induced inflammation in vivo: quantitative histomorphometric analysis of cellular events

  Arthritis and rheumatism · 2002

  📚 79 citations🎯 RCR 1.64

  Lire l'abstract Crossref ↓

  AbstractObjectiveTo quantify the inflammatory cell response in rat air pouch pseudosynovial membrane during monosodium urate monohydrate (MSU) crystal–induced inflammation.MethodsIn the rat air‐pouch model, we used a computer‐assisted histomorphometric method to quantify cell distributions, based on cell linear densities, in histologic sections of membranes from pouches injected with MSU or saline. The volume, white blood cell (WBC) count, and histamine content of the pouch exudates were determined at several time points.ResultsInjection of 10 mg of MSU crystals into the pouch produced an acute exudate. After peaking at 24 hours, the exudate volume and WBC count decreased spontaneously over the next 3 days, simulating the self‐limited course of acute gout. Membrane thickness followed a parallel course. Membrane polymorphonuclear cell (PMN) linear densities were closely correlated with exudate WBC counts, suggesting PMN recruitment from the subintimal synovial membrane. Both monocyte/macrophage and mast cell linear densities increased in the subintimal layer 2 hours after crystal injection (P = 0.038 and P = 0.03, respectively, versus controls), whereas PMN linear densities showed 2 peaks, one at 4 hours and the other 24 hours. The exudate histamine content peaked 6 hours after crystal injection, when mast cell linear densities were minimal in the membranes, suggesting mast cell degranulation.ConclusionAn increase in monocyte/macrophage and mast cell densities in the membrane preceded the PMN influx in the pouch membrane and exudate, suggesting that mast cells may be involved in the early phase of MSU crystal–induced inflammation, at least in this rat model.

• 3

  Inhibition and prevention of monosodium urate monohydrate crystal-induced acute inflammation in vivo by transforming growth factor beta1

  Arthritis and rheumatism · 1996

  📚 60 citations🎯 RCR 1.48

  Lire l'abstract Crossref ↓

  AbstractObjective. We investigated the effects of transforming growth factor β1 (TGFβ1) on monosodium urate monohydrate (MSU) crystal‐induced acute inflammation in vivo.Methods. One hour after MSU crystal–induced acute inflammation was produced in the rat subcutaneous air pouch model, the effects of recombinant human TGFβ1 (rHuTGFβ1; 10–100 pg/animal) and ultrapure TGFβ1 (UPTGFβ1; 100 and 500 pg/animal) were assessed, based on absolute and differential white blood cell counts in the exudate. The effects of 10 pg of rHuTGFβ1 preincubated with a specific anti‐TGFβ antibody, and the effects of coinjection of crystals and rHuTGFβ1, were also studied.Results. UPTGFβ1 and rHuTGFβ1 markedly reduced MSU crystal–induced inflammation. Recombinant human TGFβ1 also reduced inflammation when administered concomitantly with MSU crystals. Moreover, rHuTGFβ1 and UPTGFβ1, injected 1 hour after MSU crystal injection, reduced the inflammatory response in a dose‐dependent manner. Injection of rHuTGFβ1 (100 pg/animal) resulted in a >90% reduction in the maximal white blood cell count, achieved 6 hours after crystal injection. Preincubation of rHuTGFβ1 with a specific anti‐TGFβ1 antibody significantly (P < 0.01) reversed the inhibitory effect of rHuTGFβ1 on the inflammatory response. Consistent with the regulation of inflammatory cell recruitment into the joint, the percentage of monocytes markedly decreased (P < 0.01) following local injection with rHuTGFβ1 6 hours after MSU crystal injection.Conclusion. Exogenous TGFβ1 prevents and inhibits MSU crystal–induced acute inflammation in vivo. Its role in the self‐limitation of gouty attacks deserves consideration, among the various other factors involved.

Publications scientifiques (6) — classées par pathologie

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