Macrophage Activation after In vitro Stimulation with the TSP Antigen of Mycobacterium tuberculosis H37Rv.
- Author:
Seong Kyu PARK
;
Eun Kyeong JO
;
Jae Hyun LIM
;
Hwa Jung KIM
;
Jeong Kyu PARK
;
Tae Hyun PAIK
- Publication Type:Original Article ; In Vitro
- Keywords:
Macrophage;
Interferon-gamma Mrna expression;
Interleukin-12 Mrna expression;
Interleukin-10 Mrna expression;
TSP antigen;
Mycobacterium tuberculosis
- MeSH:
Tumor Necrosis Factor-alpha
- From:Korean Journal of Immunology
1998;20(2):141-151
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Present study aimed to investigate the immunological activities of cell wall associated protein antigen solubilized with Triton X-100 (TSP) from Mycobacterium tuberculosis H37Rv and conducted on 43 patients with pulmonary tuberculosis (newly diagnosed, medicated within 12 months and chronic refractory patients) and 17 normal healthy controls. These immunological responses were compared with those induced by the PPD or 30 kDa antigen from M, tuberculosis H37Rv culture filtrates, identified as biologically important secreted proteins. Proliferative responses to mycobacterial antigens were compared in peripheral blood mononuclear cells (PBMC) of healthy subjects and pulmonary tuberculosis patients. Signiticant blastogenic responses to the TSP were observed in healthy tuberculin reactors, newly diagnosed and some of antituberculosis drug-medicated patients by H-thymidine incorporation assay. IL-12 p40 and IFN-r mRNA expressions to the TSP were markedly increased, whereas IL-10 and TNF-a mRNA expressions were decreased at a 5 day-stimulation by PBMC in healthy tuberculin reactors, newly diagnosed and medicated patients. However, patients with chronic refractory tuberculosis exhibited more depressed IL-12 p40 and IFN-r mRNA expressions to all of the antigens than another groups. Interestingly, very low IL-10 and TNF-a mRNA expressions cultured with the TSP were also shown. These data suggest that the TSP may be involved in the macrophage activation by induction of Th1 stimulatory signals, such as IL-12, and suppression of Th1 inhibitory cytokine, IL-10.
