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Article: Changes of cytokine profiles during peritonitis in patients on continuous ambulatory peritoneal dialysis

TitleChanges of cytokine profiles during peritonitis in patients on continuous ambulatory peritoneal dialysis
Authors
KeywordsBasic fibroblast growth factor (FGF)
Continuous ambulatory peritoneal dialysis (CAPD)
Interleukin-1 (IL-1)
Interleukin-6 (IL-6)
Macrophages
Mesothelial cells
Peritonitis
Transforming growth factor-β (TGF-β)
Issue Date2000
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/ajkd
Citation
American Journal Of Kidney Diseases, 2000, v. 35 n. 4, p. 644-652 How to Cite?
AbstractContinuous ambulatory peritoneal dialysis (CAPD) has emerged as an important dialysis treatment modality worldwide. One of the major complications is bacterial peritonitis, which may result in subsequent technique failure because of loss of peritoneal clearance or peritoneal fibrosis. Bacterial peritonitis leads to the release of proinflammatory cytokines from resident and infiltrating cells in the peritoneal cavity. We studied 35 patients undergoing CAPD with acute bacterial peritonitis. All patients treated with antibiotics for 2 weeks after the clinical diagnosis of peritonitis had a good recovery. Peritoneal dialysate effluent (PDE) was collected on days 1, 3, 5, 10, 21, and 42 after the start of treatment. Cell populations were monitored by flow cytometry. PDE levels of interleukin-1β (IL-1), IL-6, transforming growth factor-β (TGF-β), and basic fibroblast growth factor (FGF) were measured by enzyme-linked immunosorbent assay. Gene transcription of TGF-β in macrophages from PDE was measured by quantitative polymerase chain reaction. Bacterial peritonitis was associated with a sharp increase in total cell and neutrophil counts (400-fold) in PDE up to 3 weeks after peritonitis despite clinical remission (P < 0.0001). There was an increased absolute number of macrophages during the first 3 weeks despite the reduced percentage of macrophages among total cells in PDE compared with noninfective PDE. There was a progressive increase in the percentage of mesothelial cells or dead cells in the total cell population in PDE over the entire 6-week period. PDE levels of IL-1, IL-6, TGF-β, and FGF increased markedly on day I before their levels decreased gradually. PDE levels of these cytokines or growth factors were significantly greater than those in noninfective PDE (n = 76) throughout the study period (P < 0.01). Similarly, TGF-β complementary DNA (cDNA) molecules per macrophage were significantly greater than those of macrophages in noninfective PDE throughout this period (P < 0.01). There was no significant correlation between PDE levels of TGF-β and TGF-β cDNA molecules per macrophage, suggesting that peritoneal macrophages are not the only source of TGF-β in PDE. We conclude there is an active release of proinflammatory cytokines and sclerogenic growth factors through at least 6 weeks despite apparent clinical remission of peritonitis. The peritoneal cytokine networks after peritonitis may potentially affect the physiological properties of the peritoneal membrane. (C) 2000 by the National Kidney Foundation, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/76676
ISSN
2015 Impact Factor: 6.269
2015 SCImago Journal Rankings: 2.313
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorLai, KBen_HK
dc.contributor.authorLam, CWKen_HK
dc.contributor.authorChan, TMen_HK
dc.contributor.authorLi, FKen_HK
dc.contributor.authorLeung, JCKen_HK
dc.date.accessioned2010-09-06T07:23:45Z-
dc.date.available2010-09-06T07:23:45Z-
dc.date.issued2000en_HK
dc.identifier.citationAmerican Journal Of Kidney Diseases, 2000, v. 35 n. 4, p. 644-652en_HK
dc.identifier.issn0272-6386en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76676-
dc.description.abstractContinuous ambulatory peritoneal dialysis (CAPD) has emerged as an important dialysis treatment modality worldwide. One of the major complications is bacterial peritonitis, which may result in subsequent technique failure because of loss of peritoneal clearance or peritoneal fibrosis. Bacterial peritonitis leads to the release of proinflammatory cytokines from resident and infiltrating cells in the peritoneal cavity. We studied 35 patients undergoing CAPD with acute bacterial peritonitis. All patients treated with antibiotics for 2 weeks after the clinical diagnosis of peritonitis had a good recovery. Peritoneal dialysate effluent (PDE) was collected on days 1, 3, 5, 10, 21, and 42 after the start of treatment. Cell populations were monitored by flow cytometry. PDE levels of interleukin-1β (IL-1), IL-6, transforming growth factor-β (TGF-β), and basic fibroblast growth factor (FGF) were measured by enzyme-linked immunosorbent assay. Gene transcription of TGF-β in macrophages from PDE was measured by quantitative polymerase chain reaction. Bacterial peritonitis was associated with a sharp increase in total cell and neutrophil counts (400-fold) in PDE up to 3 weeks after peritonitis despite clinical remission (P < 0.0001). There was an increased absolute number of macrophages during the first 3 weeks despite the reduced percentage of macrophages among total cells in PDE compared with noninfective PDE. There was a progressive increase in the percentage of mesothelial cells or dead cells in the total cell population in PDE over the entire 6-week period. PDE levels of IL-1, IL-6, TGF-β, and FGF increased markedly on day I before their levels decreased gradually. PDE levels of these cytokines or growth factors were significantly greater than those in noninfective PDE (n = 76) throughout the study period (P < 0.01). Similarly, TGF-β complementary DNA (cDNA) molecules per macrophage were significantly greater than those of macrophages in noninfective PDE throughout this period (P < 0.01). There was no significant correlation between PDE levels of TGF-β and TGF-β cDNA molecules per macrophage, suggesting that peritoneal macrophages are not the only source of TGF-β in PDE. We conclude there is an active release of proinflammatory cytokines and sclerogenic growth factors through at least 6 weeks despite apparent clinical remission of peritonitis. The peritoneal cytokine networks after peritonitis may potentially affect the physiological properties of the peritoneal membrane. (C) 2000 by the National Kidney Foundation, Inc.en_HK
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/ajkden_HK
dc.relation.ispartofAmerican Journal of Kidney Diseasesen_HK
dc.subjectBasic fibroblast growth factor (FGF)en_HK
dc.subjectContinuous ambulatory peritoneal dialysis (CAPD)en_HK
dc.subjectInterleukin-1 (IL-1)en_HK
dc.subjectInterleukin-6 (IL-6)en_HK
dc.subjectMacrophagesen_HK
dc.subjectMesothelial cellsen_HK
dc.subjectPeritonitisen_HK
dc.subjectTransforming growth factor-β (TGF-β)en_HK
dc.subject.meshBacterial Infections - etiology - metabolismen_HK
dc.subject.meshCytokines - analysisen_HK
dc.subject.meshDNA, Complementary - analysisen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshFibroblast Growth Factor 2 - analysisen_HK
dc.subject.meshFibrosis - etiology - metabolismen_HK
dc.subject.meshFlow Cytometryen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInterleukin-1 - analysisen_HK
dc.subject.meshInterleukin-6 - analysisen_HK
dc.subject.meshMacrophages, Peritoneal - chemistryen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPeritoneal Dialysis, Continuous Ambulatory - adverse effectsen_HK
dc.subject.meshPeritoneal Diseases - etiology - metabolismen_HK
dc.subject.meshPeritonitis - etiology - metabolismen_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshTransforming Growth Factor beta - analysis - geneticsen_HK
dc.titleChanges of cytokine profiles during peritonitis in patients on continuous ambulatory peritoneal dialysisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0272-6386&volume=35&issue=4&spage=644&epage=652&date=2000&atitle=Changes+of+cytokine+profiles+during+peritonitis+in+patients+on+continuous+ambulatory+peritoneal+dialysisen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailChan, TM: dtmchan@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityChan, TM=rp00394en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid10739785-
dc.identifier.scopuseid_2-s2.0-0034110753en_HK
dc.identifier.hkuros50615en_HK
dc.identifier.volume35en_HK
dc.identifier.issue4en_HK
dc.identifier.spage644en_HK
dc.identifier.epage652en_HK
dc.identifier.isiWOS:000086223700012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridLai, KB=7402135525en_HK
dc.identifier.scopusauthoridLam, CWK=8531362100en_HK
dc.identifier.scopusauthoridChan, TM=7402687700en_HK
dc.identifier.scopusauthoridLi, FK=8219093900en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK

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