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Pulmonary tuberculosis is characterized by granulomatous inflammation with an extensive infiltration of mononuclear phagocytes, but the mechanisms of phagocyte recruitment to the pleural space is unknown. In this study, pleural fluid from patients with tuberculosis contained significantly (P&lt;.001) more biologically active MIP-1alpha and MCP-1 (C-C cytokines) than did effusions from patients with congestive heart failure. Antigenic MIP-1alpha and MCP-1 was detected by immunocytochemistry in pleural biopsy sections of patients with tuberculous pleurisy. In vitro, pleural mesothelial cells stimulated with bacille Calmette-Guérin (BCG) or interferon (IFN)-gamma produced MIP-1alpha and MCP-1. Reverse transcription-polymerase chain reaction studies confirmed that both BCG and IFN-gamma induced MIP-1alpha and MCP-1 expression in mesothelial cells, demonstrating that mesothelial cell-derived C-C chemokines play a biologically important role in the recruitment of mononuclear cells to the pleural space.

Mycobacterium‐Mediated Chemokine Expression in Pleural Mesothelial Cells: Role of C‐C Chemokines in Tuberculous Pleurisy