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目的：比较研究水溶性多糖(FI0-c)及其氯磺酸修饰产物(FI0-c-S)对人炎症性细胞因子产生的影响.方法：应用氯磺酸修饰法对多糖进行化学修饰.用放射免疫分析法(RIA)及逆转录聚合酶链反应(RT-PCR)测FI0-c和FFI0-c-S对人组织瘤细胞(THP-1)和人外周血单核细胞(PBMC)分泌各种与炎症有关的细胞因子，白介素-1(IL-lα)和肿瘤坏死因子α(TNFα)的影响及对mRNA表达的影响.结果：FI0-c和FI0-c-S(浓度分别为4，40，400 mg/L)显著提高低剂量组IPS 10 mg/L协同PMA 200 nmol/L诱导的THP-1细胞产生TNFα的量，然而，这些多糖明显地抑制高剂量组LPS 100 mg/L协同PMA诱导的THP-l细胞产生TNFα.在无刺激的条件下HI0-c能够诱导比较多量的IL-lα产生，但是FI0-c或FI0-c-S却都明显抑制高剂量或低剂量LPS和PMA诱导的THP-l细胞产生IL-lα.低浓度FI0-c 4 mg/L显著抑制高剂量组LPS100 mg/L协同PMA诱导的THP-1细胞产生IL-l或TNFα mRNA及蛋白质的量.结论：松杉灵芝菌丝体水溶性多糖在不同的刺激条件下具有双向免疫调节作用.化学修饰的多糖可改变原多糖对细胞因子产生的调节方向.“,”AIM: To study the effects of water-soluble polysaccharides, FI0-C, and its sulfated derivative, FI0-c-S, on production of human proinflammatory cytokines, interleukinlα (IL-lα) and tumor necrosis factor α (TNFα).METHODS: The herbal polysaccharides were modified by chlorosulfomic acid in dimethyl sulfoxide (Me2SO). Cytokine production was measured by radioimmunoassay. mRNA for the cytokines was measured by semi-quantitative RT-PCR. RESULTS: FI0-c 4 mg/L itself induced IL-lα production by THP-1 cells without stimulants, such as lipopolysaccharides (LPS) and phorbol myristate acetate (PMA). On the other hand, FI0-c and FI0-c-S inhibited the IL-lα production by THP-1 cells with these stimulants. FI0-c and FI0-c-S significantly upregulated TNFα production by THP-1 cells without stimulants or at a low dose of LPS 10 mg/L and PMA 200 nmol/L, whereas these polysacchaddes markedly downregulated the TNFα production by a high dose of LPS 100 mg/L and PMA. Human peripheral blood mononuclear cells (PBMC) responded to FI0-c and FI0-c-S in IL-lα and TNFα production in a fashion similar to THP-1 cell responses. FI0-c 4 mg/L downregulated high-dose LPS-and PMA-induced IL-lα or TNFα mRNA and their protein production by THP-1 cells. CONCLUSION: The water-soluble polysaccharides of Ganoderma tsugae mycelium have bidirectional immunomodulatory effects on cytokine production in different cell stimulatory conditions. Chemical modification of this polysaccharide changed the intensity of regulatory effect on cytokine production.