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Article: Heat-aggregated IgA prepared from patients with IgA nephropathy increases priming of human neutrophils to produce inositol triphosphate following FMet-Leu-Phe stimulation in vitro

TitleHeat-aggregated IgA prepared from patients with IgA nephropathy increases priming of human neutrophils to produce inositol triphosphate following FMet-Leu-Phe stimulation in vitro
Authors
KeywordsHeat-aggregated IgA
IgA
IgA nephropathy
IgG
Inositol triphosphate
Neutrophils
Signal transduction
Issue Date1995
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NEF
Citation
Nephron, 1995, v. 69 n. 1, p. 1-8 How to Cite?
AbstractIt is envisaged that circulating IgA complexes play a primary role in the glomerular injury of IgA nephropathy, the most common glomerulonephritis worldwide. In this study, we examined the pathophysiological effects of IgA and IgG isolated from IgA-nephritic patients on the signal transduction of human neutrophils. Heat-aggregated forms and monomers of IgA and IgG were prepared from sera of 11 IgA-nephritic patients and 11 healthy controls. Signal transduction was studied by measuring the inositol triphosphate (IP3) production in neutrophils incubated with the immunoglobulin preparations. Different forms of IgA or IgG from IgA-nephritic patients failed to induce a significant increase in IP3 production directly as compared with control IgA or IgG. However, neutrophils preincubated with heat-aggregated IgA (HAA) from IgA-nephritic patients demonstrated a significant rise in IP3 production upon subsequent stimulation by a chemotactic peptide, FMet-Leu-Phe (FMLP); a similar finding was not observed with heat-aggregated IgG. HAA pretreatment of neutrophils increased FMLP-induced IP3 production in a dose-dependent manner. The raised IP3 production was not due to increased FMLP receptors, as HAA preincubation of neutrophils did not increase the binding of tritiated FMLP. The increased IP3 production upon FMLP stimulation in HAA-primed neutrophils was completely abolished by pertussis toxin in a dose-dependent manner. These findings tend to refute a direct stimulatory effect of HAA on phospholipase C, but, instead, may suggest that HAA prepared from IgA-nephritic patients upregulates the activation of G proteins in the plasma membrane. Our data suggest that HAA prepared from IgA-nephritic patients exert an upregulatory effect on signal transduction in neutrophils. These findings indirectly support the view that neutrophils are activated in IgA nephropathy and that they may play a contributory role in the inflammatory process of glomerular and interstitial injury.
Persistent Identifierhttp://hdl.handle.net/10722/162068
ISSN
2023 SCImago Journal Rankings: 0.774
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorLi, PKTen_HK
dc.date.accessioned2012-09-05T05:17:02Z-
dc.date.available2012-09-05T05:17:02Z-
dc.date.issued1995en_HK
dc.identifier.citationNephron, 1995, v. 69 n. 1, p. 1-8en_HK
dc.identifier.issn0028-2766en_HK
dc.identifier.urihttp://hdl.handle.net/10722/162068-
dc.description.abstractIt is envisaged that circulating IgA complexes play a primary role in the glomerular injury of IgA nephropathy, the most common glomerulonephritis worldwide. In this study, we examined the pathophysiological effects of IgA and IgG isolated from IgA-nephritic patients on the signal transduction of human neutrophils. Heat-aggregated forms and monomers of IgA and IgG were prepared from sera of 11 IgA-nephritic patients and 11 healthy controls. Signal transduction was studied by measuring the inositol triphosphate (IP3) production in neutrophils incubated with the immunoglobulin preparations. Different forms of IgA or IgG from IgA-nephritic patients failed to induce a significant increase in IP3 production directly as compared with control IgA or IgG. However, neutrophils preincubated with heat-aggregated IgA (HAA) from IgA-nephritic patients demonstrated a significant rise in IP3 production upon subsequent stimulation by a chemotactic peptide, FMet-Leu-Phe (FMLP); a similar finding was not observed with heat-aggregated IgG. HAA pretreatment of neutrophils increased FMLP-induced IP3 production in a dose-dependent manner. The raised IP3 production was not due to increased FMLP receptors, as HAA preincubation of neutrophils did not increase the binding of tritiated FMLP. The increased IP3 production upon FMLP stimulation in HAA-primed neutrophils was completely abolished by pertussis toxin in a dose-dependent manner. These findings tend to refute a direct stimulatory effect of HAA on phospholipase C, but, instead, may suggest that HAA prepared from IgA-nephritic patients upregulates the activation of G proteins in the plasma membrane. Our data suggest that HAA prepared from IgA-nephritic patients exert an upregulatory effect on signal transduction in neutrophils. These findings indirectly support the view that neutrophils are activated in IgA nephropathy and that they may play a contributory role 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.subjectHeat-aggregated IgAen_HK
dc.subjectIgAen_HK
dc.subjectIgA nephropathyen_HK
dc.subjectIgGen_HK
dc.subjectInositol triphosphateen_HK
dc.subjectNeutrophilsen_HK
dc.subjectSignal transductionen_HK
dc.subject.meshAmino Acid Sequenceen_US
dc.subject.meshGlomerulonephritis, Iga - Blood - Etiologyen_US
dc.subject.meshHeatingen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunoglobulin A - Blood - Pharmacology - Physiologyen_US
dc.subject.meshInositol 1,4,5-Trisphosphate - Biosynthesisen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshN-Formylmethionine Leucyl-Phenylalanine - Metabolism - Pharmacologyen_US
dc.subject.meshNeutrophil Activation - Drug Effects - Physiologyen_US
dc.subject.meshNeutrophils - Drug Effects - Metabolismen_US
dc.subject.meshPertussis Toxinen_US
dc.subject.meshSignal Transduction - Drug Effects - Physiologyen_US
dc.subject.meshStimulation, Chemicalen_US
dc.subject.meshUp-Regulation - Drug Effectsen_US
dc.subject.meshVirulence Factors, Bordetella - Pharmacologyen_US
dc.titleHeat-aggregated IgA prepared from patients with IgA nephropathy increases priming of human neutrophils to produce inositol triphosphate following FMet-Leu-Phe stimulation 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.doi10.1159/000188352-
dc.identifier.pmid7891778en_HK
dc.identifier.scopuseid_2-s2.0-0028860352en_HK
dc.identifier.volume69en_HK
dc.identifier.issue1en_HK
dc.identifier.spage1en_HK
dc.identifier.epage8en_HK
dc.identifier.isiWOS:A1995PY97800001-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridLi, PKT=25928016800en_HK
dc.identifier.issnl0028-2766-

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