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KMID : 0352019920170010229
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Kyung Hee University Medical Journal
1992 Volume.17 No. 1 p.229 ~ p.242
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Production of Tumor Necrosis Factor Alpha by Peripheral Blood Monocyte and Alveolar Macrophage From Patients with Pulmonary Tuberculosis
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Abstract
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TNF-α is a mononuclear phagocyte-derived mediator with a broad range of physiologic and immunologic processes. It is the essential inflammatory mediator in antibacterial resistance against diverse organisms including facultative intracellular
organisms.
Alveolar macrophages were known to produce 3 to 0 times more TNF than blood monocytes upon lipopolysaccharide stimulation. And it was reported that the capacity of TNF production of monocytes from chronic refractory tuberculosis patients was
decreased
compared with monocytes of newly diagnosed active pulmonary tuberculosis.
To investigate whether the capacity of TNF production by monocytes or macrophages is related to the disease activity in pulmonary tuberculosis, the capacity of TNF production by blood monocytes and alveolar macrophages which were obtained from
both
of
tuberculous lesion and normal area by bronchoalveolar lavage were measured in 7 patients of newly diagnosed pulmonary tuberculosis and in 6 patients of inactive pulmonary tuberculosis.
@ES The results were as follows :
@EN 1. Total cell yield, cell concentration, viability, and macrophage separation percentage of BAL fluid from normal areas were not significantly different from those from tuberculous lesion in active pulmonary tuberculosis subjects.
2. Alveolar macrophages from the tuberculous lesion released significantly greater amount of TNF in vitro in response to lipopolysaccharide than blood monocytes in active pulmonary tuberculosis (p<0.05).
3. The capacity of TNF production of alveolar macrophages from the tuberculous lesion was not
significantly different from that of alveolar macrophages from the normal areas in active pulmonary tuberculosis.
4. The capacity of TNF production of alveolar macrophages from the active lesion was enhanced than that of inactive lesion (P<0.05).
5. The ratios of TNF production of alveolar macrophages from tuberculous lesion and from normal areas to that of blood monocytes in active pulmonary tuberculosis were significantly higher than those in inactive pulmonary tuberculosis (P<0.05).
6. There was no difference in TNF production between blood monocytes and alveolar macrophages in inactive disease.
In conclusion, the levels of TNF produced by alveolar macrophages was related to the disease activity of pulmonary tuberculosis in this study, and the enhanced TNF production by alveolar macrophages in patients with active pulmonary tuberculosis
may
suggest the activation of local immune response in the lung.
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KEYWORD
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