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      Relationship between Mast Cells in the Tubulointerstitium and Prognosis of Patients with IgA Nephropathy

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          Abstract

          There have been a few reports suggesting that mast cells may play an important role in the development of fibrosis and/or the degradation of extracellular matrix. We examined the relationship between the number of distribution of mast cells in tubulointerstitium and prognosis of patients with IgA nephropathy. Renal biopsy specimens were stained with mouse monoclonal antihuman mast cell tryptase antibody and then with aniline blue. Specimens from 45 patients with IgA nephropathy and from 5 patients with minimal-change nephrotic syndrome were used. There was a significant correlation between the number of mast cells per unit area of the whole tubulointerstitium and the degree of tubulointerstitial fibrosis or renal function. Patients with IgA nephropathy were divided into two groups (group 1: ‘minimal’ and ‘slight’; group 2: ‘moderate’ and ‘advanced’) according to the classification by a previously reported method. Mast cells were mainly observed in the fibrotic areas in group 1. In group 2, many mast cells were detected not only in the fibrotic but also in the nonfibrotic areas. It appears that the number of mast cells in the nonfibrotic areas may be one of the predictive factors for the prognosis of patients with IgA nephropathy.

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          Most cited references 6

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          Mast cells as a source of both preformed and immunologically inducible TNF-alpha/cachectin.

          Tumour necrosis factor-alpha (TNF-alpha)/cachectin is a multifunctional cytokine that has effects in inflammation, sepsis, lipid and protein metabolism, haematopoiesis, angiogenesis and host resistance to parasites and malignancy. TNF-alpha was first described in activated macrophages, but certain mouse or rat mast cell populations (reviewed in refs 4,5) and some in vitro-derived human cells with cytochemical features of mast cells-basophils may also contain products similar to TNF-alpha. Here we present evidence that resident mouse peritoneal mast cells constitutively contain large amounts of TNF-alpha bioactivity, whereas cultured, immature mast cells vary in their TNF-alpha content. IgE-dependent activation of cultured or peritoneal mast cells induces extracellular release of TNF-alpha and augments levels of TNF-alpha messenger RNA and bioactivity. These findings identify mouse mast cells as an important source of both preformed and immunologically inducible TNF-alpha, and suggest that release of TNF-alpha by mast cells may contribute to host defence, the pathophysiology of allergic diseases and other processes dependent on TNF-alpha.
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            New concepts about the mast cell.

             S Galli (1993)
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              Inflammatory cells and mediators in bronchial lavage of patients with chronic obstructive pulmonary disease.

              Cigarette smoking is the most important cause of chronic obstructive pulmonary disease (COPD). Although the precise sequence of events that leads a smoker to experience airway obstruction is not completely clear, airway inflammation is a relevant factor. To investigate airway inflammation, 12 nonatopic smoking COPD patients with a forced expiratory volume in one second (FEV1) < or = 75% predicted and 10 normal nonsmoking subjects (NS) were studied with bronchoscopy and bronchial lavage (BL). Serum immunoglobulin (Ig)E levels of COPD patients correlated with the smoking history (r=0.7, p=0.008). In BL of COPD patients there was an increase of neutrophils (median, range) (COPD 62.6x10(3), 1.2-323, NS 1.35, 0-19.2, p=0.001), eosinophils (COPD 1.6, 0-6.9, NS 0.15, 0-3.7, p=0.035), the levels of interleukin (IL)-8 (COPD 1079 pg x mL(-1), 121-2,500, NS 20.4, 7.2-59, p=0.001), myeloperoxidase (MPO) (COPD 752 microg x L(-1), 11-5,500, NS 22.1, 8-70, p=0.001) and eosinophil cationic protein (ECP) (COPD 21.5 microg x L(-1), 1.8-161, NS 2, 1.8-4.9, p=0.001). Significant correlations were found in BL of COPD patients between IL-8 and neutrophils (p=0.02), MPO and neutrophils (p=0.02), IL-8 and MPO (p=0.0001) and ECP and eosinophils (p=0.02). In addition, the ratios between the BL levels of MPO and the number of neutrophils and between ECP levels and eosinophils were higher in COPD patients than in NS (p=0.03 and 0.01, respectively). These data suggest that cigarette smoke is associated with increased amounts of airway interleukin-8, a chemotactic factor for neutrophils and eosinophils. Recruited neutrophils and eosinophils are activated and they release increased amounts of inflammatory mediators capable of damaging the bronchial tissue.
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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                2001
                2001
                22 November 2001
                : 89
                : 4
                : 391-397
                Affiliations
                Division of Nephrology, Department of Medicine, Juntendo University School of Medicine, Tokyo, Japan
                Article
                46109 Nephron 2001;89:391–397
                10.1159/000046109
                11721155
                © 2001 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: 5, Tables: 2, References: 35, Pages: 7
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/46109
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