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      Increased Migratory and Activation Cell Markers of Peripheral Blood Lymphocytes in an Experimental Model of Nephrotic Syndrome

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          Abstract

          The present study aimed to evaluate the expression of CD80 and CD18 in subpopulations of peripheral blood leukocytes and oxidative kidney damage in rats with nephrotic syndrome (NS) induced by doxorubicin (Dox) in comparison to control animals at different time points. Male adult Wistar rats were submitted to 24-hour urine and blood collection for biochemical and immunological analysis at 7, 14, 21, and 28 days after Dox injection. After euthanasia, the kidneys were removed for histological analysis and the evaluation of oxidative stress. The phenotypic characterization of leukocytes was performed using flow cytometry. Dox-injected animals exhibited increased CD18 expression in cytotoxic T lymphocytes, NK cells, and monocytes and high CD80 expression in monocytes. Kidney oxidative damage was positively correlated with CD80 expression in monocytes and serum levels of creatinine. These results suggest that phagocytic and cytotoxic cells are preferentially recruited to the tissue injury site, which may contribute to kidney dysfunction in this animal model of NS. The blockade of integrin and costimulatory molecules may provide new therapeutic opportunities for NS.

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          Integrin ligands at a glance.

          Jonathan Humphries, Adam Byron, Martin J. Humphries (2006)
          Article 0 comments Cited 452 times – based on 0 reviews     Review now
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            Adriamycin nephropathy: a model of focal segmental glomerulosclerosis.

            David C H Harris, S Lee (2010)
            Adriamycin nephropathy (AN) is a rodent model of chronic kidney disease that has been studied extensively and has enabled a greater understanding of the processes underlying the progression of chronic proteinuric renal disease. AN is characterized by podocyte injury followed by glomerulosclerosis, tubulointerstitial inflammation and fibrosis. Genetic studies have demonstrated a number of loci that alter both risk and severity of renal injury induced by Adriamycin. Adriamycin-induced renal injury has been shown in numerous studies to be modulated by both non-immune and immune factors, and has facilitated further study of mechanisms of tubulointerstitial injury. This review will outline the pharmacological behaviour of Adriamycin, and describe in detail the model of AN, including its key structural characteristics, genetic susceptibility and pathogenesis. © 2011 The Authors. Nephrology © 2011 Asian Pacific Society of Nephrology.
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              Ex vivo programmed macrophages ameliorate experimental chronic inflammatory renal disease.

              Y. WANG, G. Zheng, V W S Lee … (2007)
              Macrophage infiltration of the kidney is a prominent feature associated with the severity of renal injury and progressive renal failure. To determine the influence of macrophages in renal disease models in the absence of endogenous T and B cells, we performed adoptive transfer of macrophages into severe combined immunodeficient (SCID) mice. In this study, macrophages were isolated from the spleens of BALB/c mice and stimulated with lipopolysaccharide to induce classically activated M1 macrophages or with interleukin-4 (IL-4) and IL-13 to induce alternatively activated M2 macrophages. These macrophages were then infused into SCID mice with adriamycin nephropathy; an in vivo model of chronic inflammatory renal disease analogous to human focal segmental glomerulosclerosis. Mice infused with M1 macrophages had a more severe histological and functional injury, whereas M2 macrophage-induced transfused mice had reduced histological and functional injury. Both M1 and M2 macrophages localized preferentially to the area of injury and maintained their phenotypes even after 4 weeks. The protective effect of M2 macrophages was associated with reduced accumulation and possibly downregulated chemokine and inflammatory cytokine expression of the host infiltrating macrophages. Our findings demonstrate that macrophages not only act as effectors of immune injury but can be induced to provide protection against immune injury.
              Article 0 comments Cited 111 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mediators Inflamm
                Journal ID (iso-abbrev): Mediators Inflamm
                Journal ID (publisher-id): MI
                Title: Mediators of Inflammation
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 0962-9351
                ISSN (Electronic): 1466-1861
                Publication date (Print): 2015
                Publication date (Electronic): 7 May 2015
                Volume: 2015
                Electronic Location Identifier: 209764
                Affiliations
                1Immunology Laboratory, Integrated Health Research Center, Universidade Federal dos Vales do Jequitinhonha e Mucuri (UFVJM), 38610-000 Diamantina, MG, Brazil
                2Immunopathology Laboratory, Center for Research in Biological Sciences (LIMP/NUPEB), Universidade Federal de Ouro Preto (UFOP), 30140-081 Ouro Preto, MG, Brazil
                3Interdisciplinary Laboratory of Medical Investigation, Pediatric Nephrology Unit, Universidade Federal de Minas Gerais (UFMG), 30130-100 Belo Horizonte, MG, Brazil
                Author notes
                *Ana Cristina Simões e Silva: acssilva@ 123456hotmail.com

                Academic Editor: Ronald Gladue

                Article
                DOI: 10.1155/2015/209764
                PMC ID: 4439504
                SO-VID: e54442a6-0daf-423c-955d-910158f20680
                Copyright © Copyright © 2015 Wagner de Fátima Pereira et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 6 March 2015
                Date revision received : 18 April 2015
                Date accepted : 19 April 2015
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

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