4.6 Article

Effect of vitamin D3 on phagocytic potential of macrophages with live Mycobacterium tuberculosis and lymphoproliferative response in pulmonary tuberculosis

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JOURNAL OF CLINICAL IMMUNOLOGY
卷 24, 期 3, 页码 249-257

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SPRINGER/PLENUM PUBLISHERS
DOI: 10.1023/B:JOCI.0000025446.44146.52

关键词

vit. D3; macrophages; phagocytosis; lymphoproliferation; M. tuberculosis; pulmonary TB

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Immune responses are elicited through antigen presentation and recognition by macrophages and T-lymphocytes, respectively. The immunomodulatory effect of vitamin D-3 on macrophage phagocytic potential with live Mycobacterium tuberculosis, spontaneous and M. tuberculosis culture filtrate antigen induced lymphocyte responses were studied in pulmonary tuberculosis patients (PTBPs) (n = 31) and normal healthy subjects (NHSs) (n = 43). Vitamin D-3 at a concentration of 10(-7) M significantly enhanced the macrophage phagocytosis of live M. tuberculosis in normal subjects with low phagocytic potential (less than 10%) (p = 0.015). No such increase was observed in PTBPs. Vitamin D-3 significantly decreased the spontaneous lymphoproliferative response (p = 0.022) and increased the apoptosis of peripheral blood mononuclear cells in PTBPs (p = 0.024). In normals, vitamin D-3 increased the spontaneous lymphoproliferative response. An inverse correlation between macrophage phagocytosis and spontaneous response was observed in NHSs, whereas a direct correlation was seen between vitamin D-3-treated cells in normal subjects under in vitro condition. Vitamin D-3 decreased the M. tuberculosis culture filtrate antigen induced lymphocyte response significantly in normal subjects (p = 0.0003), while it had no influence on the lymphocyte response in PTBPs. The present study suggests that exposure to vitamin D-3 increases the phagocytic potential and spontaneous lymphoproliferative response but brings down the antigen-induced response in normals. In tuberculosis, addition of vitamin D-3 has no significant effect on antigen-induced lymphoproliferative response. This may be due to the unresponsive nature of the cells to the action of vitamin D-3 by virtue of the disease, which renders them inactive.

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