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Article: Heat-Aggregated IgA prepared from patients with IgA nephropathy increases calcium mobilization superoxide production of human neutrophils in vitro

TitleHeat-Aggregated IgA prepared from patients with IgA nephropathy increases calcium mobilization superoxide production of human neutrophils in vitro
Authors
KeywordsCalcium flux
Heat-aggregated IgA
IgA nephropathy
Immunoglobulin A
Immunoglobulin G
Neutrophils
Signal transduction
Superoxide production
Issue Date1993
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NEF
Citation
Nephron, 1993, v. 64 n. 1, p. 129-135 How to Cite?
AbstractIgA nephropathy, characterized by predominant mesangial IgA deposition, is the commonest glomerulonephritis worldwide. It is envisaged that circulating IgA plays a primary role in the glomerular injury of IgA nephropathy. In this study, we examined the pathophysiologic effect of IgA and IgG isolated from IgA nephritic patients on the signal transduction and oxidative metabolism of human neutrophils. Heat-aggregated forms, monomers, and F(ab')2 fragments of IgA and IgG were prepared from sera of 11 IgA nephritic patients and 11 healthy controls. Signal transduction was studied by measuring calcium mobilization and oxidative metabolism by measuring superoxide production. Different forms of IgA and IgG from patients with IgA nephropathy did not induce a significant increase in calcium mobilization directly. Nonetheless, neutrophils preincubated with heat-aggregated IgA or IgG from IgA nephritic patients demonstrated a significant rise in calcium mobilization upon subsequent stimulation by a chemotactic peptide, FMet-Leu-Phe (FMLP). Heat-aggregated IgA or IgG pretreatment of neutrophils increased FMLP-induced calcium mobilization in a dose-dependent manner. Aggregated IgA or IgG prepared by heat aggregation from IgA nephritic patients induced a significantly greater superoxide production from neutrophils than immunoglobulins from healthy controls. Similarly, heat-aggregated IgA and IgG induced superoxide production in a dose-dependent manner. Our data suggest that heat-aggregated forms of IgA and IgG exert an upregulatory effect on signal transduction and oxidative metabolism in human neutrophils. These findings indirectly support the view that neutrophils could be activated in IgA nephropathy and may potentially be participating in the inflammatory process of glomerular and interstitial injury.
Persistent Identifierhttp://hdl.handle.net/10722/161991
ISSN
2004 Impact Factor: 1.462
2006 SCImago Journal Rankings: 0.715
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorLeung, JCKen_HK
dc.date.accessioned2012-09-05T05:16:30Z-
dc.date.available2012-09-05T05:16:30Z-
dc.date.issued1993en_HK
dc.identifier.citationNephron, 1993, v. 64 n. 1, p. 129-135en_HK
dc.identifier.issn0028-2766en_HK
dc.identifier.urihttp://hdl.handle.net/10722/161991-
dc.description.abstractIgA nephropathy, characterized by predominant mesangial IgA deposition, is the commonest glomerulonephritis worldwide. It is envisaged that circulating IgA plays a primary role in the glomerular injury of IgA nephropathy. In this study, we examined the pathophysiologic effect of IgA and IgG isolated from IgA nephritic patients on the signal transduction and oxidative metabolism of human neutrophils. Heat-aggregated forms, monomers, and F(ab')2 fragments of IgA and IgG were prepared from sera of 11 IgA nephritic patients and 11 healthy controls. Signal transduction was studied by measuring calcium mobilization and oxidative metabolism by measuring superoxide production. Different forms of IgA and IgG from patients with IgA nephropathy did not induce a significant increase in calcium mobilization directly. Nonetheless, neutrophils preincubated with heat-aggregated IgA or IgG from IgA nephritic patients demonstrated a significant rise in calcium mobilization upon subsequent stimulation by a chemotactic peptide, FMet-Leu-Phe (FMLP). Heat-aggregated IgA or IgG pretreatment of neutrophils increased FMLP-induced calcium mobilization in a dose-dependent manner. Aggregated IgA or IgG prepared by heat aggregation from IgA nephritic patients induced a significantly greater superoxide production from neutrophils than immunoglobulins from healthy controls. Similarly, heat-aggregated IgA and IgG induced superoxide production in a dose-dependent manner. Our data suggest that heat-aggregated forms of IgA and IgG exert an upregulatory effect on signal transduction and oxidative metabolism in human neutrophils. These findings indirectly support the view that neutrophils could be activated in IgA nephropathy and may potentially be participating in the inflammatory process of glomerular and interstitial injury.en_HK
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NEFen_HK
dc.relation.ispartofNephronen_HK
dc.subjectCalcium fluxen_HK
dc.subjectHeat-aggregated IgAen_HK
dc.subjectIgA nephropathyen_HK
dc.subjectImmunoglobulin Aen_HK
dc.subjectImmunoglobulin Gen_HK
dc.subjectNeutrophilsen_HK
dc.subjectSignal transductionen_HK
dc.subjectSuperoxide productionen_HK
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshGlomerulonephritis, Iga - Blood - Immunologyen_US
dc.subject.meshHot Temperatureen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunoglobulin A - Isolation & Purification - Pharmacologyen_US
dc.subject.meshImmunoglobulin Fab Fragments - Isolation & Purification - Pharmacologyen_US
dc.subject.meshImmunoglobulin G - Isolation & Purification - Pharmacologyen_US
dc.subject.meshKineticsen_US
dc.subject.meshN-Formylmethionine Leucyl-Phenylalanine - Pharmacologyen_US
dc.subject.meshNeutrophils - Drug Effects - Metabolismen_US
dc.subject.meshSignal Transduction - Drug Effectsen_US
dc.subject.meshSuperoxides - Metabolismen_US
dc.titleHeat-Aggregated IgA prepared from patients with IgA nephropathy increases calcium mobilization superoxide production of human neutrophils in vitroen_HK
dc.typeArticleen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1159/000187292-
dc.identifier.pmid8389007-
dc.identifier.scopuseid_2-s2.0-0027408692en_HK
dc.identifier.volume64en_HK
dc.identifier.issue1en_HK
dc.identifier.spage129en_HK
dc.identifier.epage135en_HK
dc.identifier.isiWOS:A1993KZ22000021-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK

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