Abstract

The role of monocyte chemotactic protein (MCP)-1 in human pulmonary and pleural tuberculosis (TB) was assessed by examining its production in clinical samples from patients with active pulmonary TB and tuberculous pleurisy (TBP). Serum was obtained from 26 active pulmonary TB patients [14 early TB (E-TB), and 12 chronic refractory TB (CR-TB)] and 15 healthy tuberculin reactors (HTRs). The monocytes and peripheral blood mononuclear cells (PBMCs) were separated and stimulated with purified protein derivatives (PPD) or the 30-kDa antigen of Mycobacterium tuberculosis. Pleural exudates were isolated from 25 patients with TBP and 24 non-TBP patients [malignancy and congestive heart failure (CHF)]. The MCP-1 levels were measured by enzyme-linked immunosorbent assay (ELISA). In sera, the MCP-1 levels of TB patients were similar to those of HTRs. For monocytes, CR-TB patients spontaneously expressed more MCP-1, compared with HTRs and E-TB patients. In addition, MCP-1 production of PPD- or 30-kDa antigen-stimulated monocytes was significantly elevated in CR-TB patients than that from E-TB. Interestingly, the E-TB patients had significantly depressed MCP-1 production by PBMCs in response to PPD or 30-kDa, compared with HTRs and CR-TB patients. In pleural effusions, MCP-1 levels were significantly higher in patients with TBP than in patients with CHF, but lower than in malignant effusions. The data suggest that MCP-1 production is not uniquely elevated systemically in TB patients, although MCP-1 production might be elevated by monocytes in the chronic phase of TB or with a local pleural infection.

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