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      Enhanced Expression of C Chemokine Lymphotactin in IgA Nephropathy

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          Abstract

          Leukocyte accumulation in the kidney is observed in patients with IgA nephropathy. Chemokines are a large family of cytokines chemotactic for leukocytes and have been shown to be upregulated in renal diseases. We previously reported that the gene expression of lymphotactin, a sole member of C chemokine subfamily, is enhanced in an animal model of crescentic glomerulonephritis, but its expression in human renal diseases is totally unknown. In the present study, we investigated the expression of mRNAs of lymphotactin and some other chemokines in IgA nephropathy. The expression of mRNAs for three chemokines, lymphotactin, MCP-1, and MIP-1β, in renal cortex was increased and the levels of lymphotactin and MCP-1 mRNAs were statistically higher in patients with glomerular crescents than in those without crescents. These levels also correlated with tubulointerstitial changes and urinary protein excretion. Glomerular levels of mRNAs for lymphotactin and MCP-1, but not MIP-1β, were higher in IgA nephropathy than controls. By immunohistochemical analysis, lymphotactin was detected in tryptase-positive cells (putative mast cells) in the interstitial space. These results suggest that lymphotactin, as well as MCP-1, may contribute to leukocyte infiltration and disease progression in IgA nephropathy.

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          Most cited references 4

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          Contribution of mast cells to the tubulointerstitial lesions in IgA nephritis.

           T Ehara,  H Shigematsu (1998)
          Mast cells have never been extensively investigated in renal disease, particularly glomerulonephritis. Recent improvements in monoclonal antibody production to mast cell specific enzymes have made it possible to study mast cells in tissues more accurately and easily. Mast cells have been found to secrete basic fibroblast growth factor (bFGF) in human pulmonary fibrosis. Mast cells in 67 cases of IgA nephritis were investigated. Toluidine blue (TB) stainings at pH 5.0 and pH 0.5 were employed histochemically, and anti-human mast cell tryptase and chymase monoclonal antibodies were used immunohistochemically. Anti-bFGF antibody was also used immunohistochemically. Mast cells were scattered in the interstitium including in fibrotic areas. TB pH 0.5-positive mast cells were more numerous than TB pH 5. 0-positive mast cells. Immunostaining with anti-tryptase monoclonal antibody detected more mast cells than the TB stainings. Mast cells in the interstitium of IgA nephritis had both tryptase and chymase. Immunoelectron microscopy showed that tryptase was exclusively localized in the specific granules of mast cells. The average number of tryptase positive mast cell in the interstitium of IgA nephritis was lower than that of T lymphocyte but more than that of macrophages. The average number of mast cells increased with the progression of interstitial fibrosis and had a significant correlation with 24-hour creatinine clearance. Using double labeled immunohistochemistry, some tryptase-positive mast cells had bFGF in their cytoplasm. Electron microscopy showed that mast cells were associated with fibroblasts and/or lymphocytes in the interstitium. Mast cells are one of the constitutive cells in the interstitium of IgA nephritis patients and affect renal function by contributing to the interstitial fibrosis.
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            • Record: found
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            Identification of Single C Motif-1/Lymphotactin Receptor XCR1

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              • Record: found
              • Abstract: not found
              • Article: not found

              Involvement of neutrophil elastase in crescentic glomerulonephritis

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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                2002
                June 2002
                03 June 2002
                : 91
                : 2
                : 262-269
                Affiliations
                aDepartment of Clinical Pharmacology, Research Institute, International Medical Center of Japan, Tokyo, and bDepartment of Nephrology, Sendai Shakaihoken Hospital, Sendai, Japan
                Article
                58402 Nephron 2002;91:262–269
                10.1159/000058402
                12053063
                © 2002 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 6, Tables: 1, References: 30, Pages: 8
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/58402
                Categories
                Original Paper

                Cardiovascular Medicine, Nephrology

                IgA nephropathy, Mast cells, MCP-1, MIP-1β, Chemokine, Lymphotactin

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