Antileukoproteinase: modulation of neutrophil function and therapeutic effects on anti-type II collagen antibody-induced arthritis

Arthritis and Rheumatism
Bettina SehnertH Burkhardt

Abstract

Antileukoproteinase (ALP) is a physiologic inhibitor of granulocytic serine proteases. The present study was undertaken to investigate its therapeutic benefit in an antibody-transfer model of erosive polyarthritis and to elucidate its potential to interfere with immune complex-dependent inflammatory pathways. Arthritis development was induced in male (BALB/c x B10.Q)F(1) mice by intravenous injection of two monoclonal antibodies specific for type II collagen and was quantified by clinical scoring and histopathology. Arthritis severity was assessed in a cohort of mice under systemic treatment with recombinant human ALP (daily doses of 0.1 mg for 5 days starting immediately after disease induction) in comparison with untreated controls. Concomitantly, functional assays (phagocytosis, oxidative burst, fluorescence-activated cell sorting analysis of integrin expression) were performed on neutrophils upon in vitro stimulation by IgG-coated latex beads. ALP treatment reduced arthritis incidence and severity and had a protective effect against cartilage and bone erosion. ALP inhibited the conversion of the leukocyte beta2 integrins into an active conformation upon Fc receptor stimulation of granulocytes. ALP bound to the actin-bundlin...Continue Reading

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Citations

Oct 15, 2010·Molecular & Cellular Proteomics : MCP·Massimo CastagnolaIrene Messana
Jun 18, 2005·Acta Pharmacologica Sinica·Veerle DelanoteJan Gettemans
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