Masoud Shamaei1, Esmaeil Mortaz2, Mihan Pourabdollah3, Johan Garssen4, Payam Tabarsi1, Aliakbar Velayati5, Ian M Adcock6. 1. Clinical Tuberculosis and Epidemiology Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran. 2. Clinical Tuberculosis and Epidemiology Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran; Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, Netherlands. 3. Chronic Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran. 4. Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, Netherlands; Nutricia Research Centre for Specialized Nutrition, Utrecht, Netherlands. 5. Mycobacteriology Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Masih Daneshvari Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran. 6. Airways Disease Section, National Heart & Lung Institute, Imperial College London, London, UK; Priority Research Centre for Healthy Lungs, Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia. Electronic address: Ian.adcock@imperial.ac.uk.
Abstract
BACKGROUND: Sarcoidosis is a granulomatous disease of unknown etiology. Macrophages play a key role in granuloma formation with the T cells, having a significant impact on macrophage polarization (M1 and M2) and the cellular composition of the granuloma. This study evaluates macrophage polarization in granulomas in pulmonary sarcoidosis. MATERIALS AND METHODS: Tissue specimens from the Department of Pathology biobank at the Masih Daneshvari Hospital were obtained. Paraffin sections from 10 sarcoidosis patients were compared with those from 12 cases of tuberculosis using immunohistochemical staining. These sections consisted of mediastinal lymph nodes and transbronchial lung biopsy (TBLB) for sarcoidosis patients versus pleural tissue, neck, axillary lymph nodes and TBLB for tuberculosis patients. The sections were stained for T-cells (CD4+, CD8+) and mature B lymphocytes (CD22+). CD14+ and CD68+ staining was used as a marker of M1 macrophages and CD163+ as a marker for M2 macrophages. RESULTS: Immunohistochemical staining revealed a 4/1 ratio of CD4+/CD8+ T-cells in sarcoidosis granuloma sections and a 3/1 ratio in tuberculosis sections. There was no significance difference in single CD4+, CD8+, CD22+, CD14+ and CD68+ staining between sarcoidosis and tuberculosis sections. CD163 expression was significantly increased in sarcoidosis sections compared with those from tuberculosis subjects. CONCLUSION: Enhanced CD163+ staining indicates a shift towards M2 macrophage subsets in granulomas from sarcoidosis patients. Further research is required to determine the functional role of M2 macrophages in the immunopathogenesis of sarcoidosis.
BACKGROUND: Sarcoidosis is a granulomatous disease of unknown etiology. Macrophages play a key role in granuloma formation with the T cells, having a significant impact on macrophage polarization (M1 and M2) and the cellular composition of the granuloma. This study evaluates macrophage polarization in granulomas in pulmonary sarcoidosis. MATERIALS AND METHODS: Tissue specimens from the Department of Pathology biobank at the Masih Daneshvari Hospital were obtained. Paraffin sections from 10 sarcoidosis patients were compared with those from 12 cases of tuberculosis using immunohistochemical staining. These sections consisted of mediastinal lymph nodes and transbronchial lung biopsy (TBLB) for sarcoidosis patients versus pleural tissue, neck, axillary lymph nodes and TBLB for tuberculosis patients. The sections were stained for T-cells (CD4+, CD8+) and mature B lymphocytes (CD22+). CD14+ and CD68+ staining was used as a marker of M1 macrophages and CD163+ as a marker for M2 macrophages. RESULTS: Immunohistochemical staining revealed a 4/1 ratio of CD4+/CD8+ T-cells in sarcoidosis granuloma sections and a 3/1 ratio in tuberculosis sections. There was no significance difference in single CD4+, CD8+, CD22+, CD14+ and CD68+ staining between sarcoidosis and tuberculosis sections. CD163 expression was significantly increased in sarcoidosis sections compared with those from tuberculosis subjects. CONCLUSION: Enhanced CD163+ staining indicates a shift towards M2 macrophage subsets in granulomas from sarcoidosis patients. Further research is required to determine the functional role of M2 macrophages in the immunopathogenesis of sarcoidosis.
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