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Article: Interaction between proximal tubular epithelial cells and infiltrating monocytes/T cells in the proteinuric state

TitleInteraction between proximal tubular epithelial cells and infiltrating monocytes/T cells in the proteinuric state
Authors
KeywordsChemokine receptor
Chemokines
Monocytes
Proteinuria
Proximal tubular epithelial cells
T cells
Issue Date2007
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.html
Citation
Kidney International, 2007, v. 71 n. 6, p. 526-538 How to Cite?
AbstractWe hypothesize an interaction between T cells/monocytes and the tubules in the development of tubulointerstitial injury in chronic proteinuric nephropathy. We established in vitro co-culture systems of proximal tubular epithelial cells (PTEC) and T cells/monocytes to study the contribution of soluble factors and cell-to-cell contact in the development of tubulointerstitial injury. The release of monocyte chemoattractant protein-1 (MCP1 or CCL2), Regulated upon Activation, normal T cell Expressed and Secreted (RANTES or CCL5), soluble intracellular adhesion molecules-1 (sICAM-1), or interleukin-6 (IL-6) was increased in PTEC following apical exposure to human serum albumin (HSA). The release of CCL2, CCL5, or sICAM-1 from PTEC was enhanced by contact of monocytes/T cells on the basolateral surface. Tumor necrosis factor-α (TNF-α) and IL-1β are important soluble factors as suggested by the blocking effect of antibodies (Abs) against TNF-α or IL-1β but not against other cytokines. The percentage of CD4+ T cells expressing both chemokine receptors, CCR2 and CCR5, was increased after culturing with supernatant from the apical or basolateral surface of PTEC following apical exposure to HSA. However, only CCR2 was upregulated in CD8+ T cells, whereas CCR5 expression was increased in monocytes. The chemotaxis of CD4+ or CD8+ T cells to supernatant from PTEC upon apical exposure to HSA was reduced with neutralizing Abs against CCL5 and/or CCL2, whereas the chemotaxis of monocytes was only reduced by anti-CCL5 but not by anti-CCL2. In summary, chemokines released by HSA-activated PTEC are amplified by monocytes/T cells. Mediators released by HSA-activated PTEC can differentially modulate the expression of chemokine receptors in monocytes/T cells and hence, alter their chemotaxis towards activated PTEC. These interactions are pivotal in the development of tubulointerstitial injury. © 2007 International Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/76427
ISSN
2015 Impact Factor: 7.683
2015 SCImago Journal Rankings: 3.181
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorGuo, Hen_HK
dc.contributor.authorTang, SCWen_HK
dc.date.accessioned2010-09-06T07:21:08Z-
dc.date.available2010-09-06T07:21:08Z-
dc.date.issued2007en_HK
dc.identifier.citationKidney International, 2007, v. 71 n. 6, p. 526-538en_HK
dc.identifier.issn0085-2538en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76427-
dc.description.abstractWe hypothesize an interaction between T cells/monocytes and the tubules in the development of tubulointerstitial injury in chronic proteinuric nephropathy. We established in vitro co-culture systems of proximal tubular epithelial cells (PTEC) and T cells/monocytes to study the contribution of soluble factors and cell-to-cell contact in the development of tubulointerstitial injury. The release of monocyte chemoattractant protein-1 (MCP1 or CCL2), Regulated upon Activation, normal T cell Expressed and Secreted (RANTES or CCL5), soluble intracellular adhesion molecules-1 (sICAM-1), or interleukin-6 (IL-6) was increased in PTEC following apical exposure to human serum albumin (HSA). The release of CCL2, CCL5, or sICAM-1 from PTEC was enhanced by contact of monocytes/T cells on the basolateral surface. Tumor necrosis factor-α (TNF-α) and IL-1β are important soluble factors as suggested by the blocking effect of antibodies (Abs) against TNF-α or IL-1β but not against other cytokines. The percentage of CD4+ T cells expressing both chemokine receptors, CCR2 and CCR5, was increased after culturing with supernatant from the apical or basolateral surface of PTEC following apical exposure to HSA. However, only CCR2 was upregulated in CD8+ T cells, whereas CCR5 expression was increased in monocytes. The chemotaxis of CD4+ or CD8+ T cells to supernatant from PTEC upon apical exposure to HSA was reduced with neutralizing Abs against CCL5 and/or CCL2, whereas the chemotaxis of monocytes was only reduced by anti-CCL5 but not by anti-CCL2. In summary, chemokines released by HSA-activated PTEC are amplified by monocytes/T cells. Mediators released by HSA-activated PTEC can differentially modulate the expression of chemokine receptors in monocytes/T cells and hence, alter their chemotaxis towards activated PTEC. These interactions are pivotal in the development of tubulointerstitial injury. © 2007 International Society of Nephrology.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.htmlen_HK
dc.relation.ispartofKidney Internationalen_HK
dc.subjectChemokine receptoren_HK
dc.subjectChemokinesen_HK
dc.subjectMonocytesen_HK
dc.subjectProteinuriaen_HK
dc.subjectProximal tubular epithelial cellsen_HK
dc.subjectT cellsen_HK
dc.subject.meshCell Communication - physiologyen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshChemokine CCL2 - genetics - metabolismen_HK
dc.subject.meshChemokine CCL5en_HK
dc.subject.meshChemokines, CC - genetics - metabolismen_HK
dc.subject.meshChemotaxis - drug effects - physiologyen_HK
dc.subject.meshCoculture Techniquesen_HK
dc.subject.meshEpithelial Cells - drug effects - metabolism - pathologyen_HK
dc.subject.meshGene Expression Regulation - drug effects - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIntercellular Adhesion Molecule-1 - genetics - metabolismen_HK
dc.subject.meshInterleukin-2 Receptor alpha Subunit - genetics - metabolismen_HK
dc.subject.meshInterleukin-6 - genetics - metabolismen_HK
dc.subject.meshKidney Tubules, Proximal - drug effects - metabolism - pathologyen_HK
dc.subject.meshMonocytes - pathology - physiologyen_HK
dc.subject.meshProteinuria - pathology - physiopathologyen_HK
dc.subject.meshReceptors, Chemokine - genetics - metabolismen_HK
dc.subject.meshSerum Albumin - pharmacologyen_HK
dc.subject.meshT-Lymphocytes - pathology - physiologyen_HK
dc.titleInteraction between proximal tubular epithelial cells and infiltrating monocytes/T cells in the proteinuric stateen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0085-2538&volume=71&spage=526&epage=538&date=2007&atitle=Interaction+between+proximal+tubular+epithelial+cells+and+infiltrating+monocytes/T+cells+in+the+proteinuric+stateen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailTang, SCW: scwtang@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityTang, SCW=rp00480en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.ki.5002091en_HK
dc.identifier.pmid17245394-
dc.identifier.scopuseid_2-s2.0-33947135427en_HK
dc.identifier.hkuros132125en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33947135427&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume71en_HK
dc.identifier.issue6en_HK
dc.identifier.spage526en_HK
dc.identifier.epage538en_HK
dc.identifier.isiWOS:000244748900011-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridChan, LYY=8108378300en_HK
dc.identifier.scopusauthoridGuo, H=55468645700en_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK
dc.identifier.citeulike3908346-

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