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Mycobacterium‐Induced Transmesothelial Migration of Monocytes into Pleural Space: Role of Intercellular Adhesion Molecule–1 in Tuberculous Pleurisy
Author(s) -
Najmunnisa Nasreen,
Kamal A. Mohammed,
Melissa J. Ward,
Veena B. Antony
Publication year - 1999
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/315057
Subject(s) - mesothelium , monocyte , intercellular adhesion molecule 1 , inflammation , cell adhesion molecule , macrophage , lipoarabinomannan , intercellular adhesion molecule , pleurisy , immunology , pleural disease , pathology , cell adhesion , medicine , mesothelial cell , microbiology and biotechnology , biology , in vitro , mycobacterium tuberculosis , cell , lung , pleural effusion , respiratory disease , tuberculosis , biochemistry
The pleural mesothelium is a dynamic cellular membrane with multiple key functions. It plays a pivotal role in pleural inflammation through its release of several cytokines and the expression of cell-surface molecules. The expression of intercellular adhesion molecule (ICAM)-1 in the pleural mesothelium of patients with active pleural tuberculosis and the role of ICAM-1 in monocyte transmigration across pleural mesothelium during tuberculous inflammation was investigated. Results indicate pleural mesothelial cells (PMCs) express ICAM-1 in tuberculous pleuritis. When PMCs were stimulated with bacille Calmette-Guérin (BCG) in vitro, they expressed ICAM-1 in a time-dependent manner. Monocyte transmigration was higher across PMC monolayers that had been stimulated with BCG. Blocking ICAM-1 on BCG-activated PMC monolayers inhibited monocyte transmigration against chemotactic gradient generated by macrophage inflammatory protein 1-alpha or monocyte chemotactic protein-1. These results indicate that ICAM-1 expression in PMCs facilitates monocyte transmigration during tuberculous pleural inflammation.

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