Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/45325
Title: The role of tubulointerstitial inflammation in the progression of chronic renal failure
Author: Trujillo-Ochoa, J.L.
Corral-Jara, K.F.
Escobedo-Melendez, G.
Realpe, M.
Panduro-Cerda, Arturo
Roman, S.
Fierro, N.A.
Issue Date: 2015
Abstract: We determined the serum IgE levels and T-helper (Th)17-related cytokines during distinct hepatitis A virus (HAV)-induced clinical courses in children. A significantly higher concentration of macrophage inflammatory protein 3?, interleukin (IL)-17E and IL-17F in HAV-infected children with intermediate liver injury compared with those with minor liver damage was found. A reduction in the IgE levels in those patients who showed the highest levels of IL-17F in the group of intermediate liver injury was found. The data suggested that the Th17-related profile is associated with the severity of HAV infection and might play a role on the modulation achieved by HAV during allergies. " 2015, Fundacao Oswaldo Cruz. All rights reserved.",,,,,,"10.1590/0074-02760140309",,,"http://hdl.handle.net/20.500.12104/45325","http://www.scopus.com/inward/record.url?eid=2-s2.0-84926332976&partnerID=40&md5=eadba30382867ee247c0d2a05a328f02
http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&D=prem&AN=25946253",,,,,,"2",,"Memorias do Instituto Oswaldo Cruz",,"263
266",,"110",,"Scopus
WOS
MEDLINE",,,,"Index Medicus",,"Cytokines; Hepatitis A virus; IgE; Th17",,,,,,"T-helper 17-related cytokines and IgE antibodies during hepatitis A virus infection in children",,"Article" "47054","123456789/35008",,"Rodríguez-Iturbe, B., Instituto Venezolano de Investigaciones Científicas (IVIC-Zulia), Universidad Del Zulia and Centro de Investigaciones Biomédicas, Hospital Universitario de Maracaibo, Maracaibo, Venezuela, Servicio de Nefrología, Hospital Universitario de Maracaibo, Ave Goajira s/n, Maracaibo 4001-A, Venezuela; García García, G., Servicio de Nefrología, Antiguo Hospital Civil de Guadalajara, Universidad de Guadalajara, Guadalajara, Mexico",,"Rodriguez-Iturbe, B.
García García, G.",,"2010",,"There is compelling evidence that interstitial inflammation plays a central role in the loss of renal function in chronic renal disease. The combined effects of interstitial inflammation, oxidative stress and local angiotensin II activity result in the disruption of glomerulus-tubule continuity, the development of pathogenic hypoxia, the generation of myofibroblasts and fibrosis, and the impairment of the protective autoregulation of glomerular blood flow that leads to glomerulosclerosis. The association between proteinuria and progression of chronic kidney disease is firmly established. Proximal tubular cells (PTC) exposed to high concentration of proteins produce proinflammatory and profibrotic factors. The activation of nuclear factor ?B and the signal transducer and activator of transcription results in the upregulation of a variety of cytokines and chemokines, overexpression of adhesion molecules and interstitial infiltration of inflammatory cells. Fibrosis is promoted by release of transforming growth factor ?, which induces myofibroblast formation and collagen deposition. Finally, the participation of vitamin D3 deficiency in the development of tubulointerstitial fibrosis is reviewed. The molecule 1,25-(OH)2D3 modulates PTC proliferation, suppresses fibroblast activation and matrix production, reduces epithelial mesenchymal transition and downregulates the genes of the renin-angiotensin system, which are critical steps in the development of a scarred kidney. Copyright " 2010 S. Karger AG, Basel.
URI: http://hdl.handle.net/20.500.12104/45275
http://www.scopus.com/inward/record.url?eid=2-s2.0-77952477767&partnerID=40&md5=abef138bfd9203f1aecf0b81a6cf04fa
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