Sakurai T, Ohno N, Suzuki I, Yadomae T
Laboratory of Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science, Japan.
Immunopharmacology. 1995 Aug;30(2):157-66. doi: 10.1016/0162-3109(95)00019-p.
In this study, we examined the effect of systemic administration of SSG, a soluble highly branched (1-->3)-beta-D-glucan obtained from a fungus Sclerotinia sclerotiorum IFO 9395, on pulmonary immune responses in mice. SSG (10 mg/kg) administered intravenously (i.v.) rapidly leaked into the alveolar space and enhanced several functions of alveolar macrophages (AMs), such as phagocytic activity, lysosomal enzyme activity, active oxygen secretion and cytokine production, on day 1 post-administration. However, kinetic changes of influx of SSG into alveoli and AM activation after SSG treatment were different. The enhanced AM functions decreased to control value on day 2 when SSG still existed at the alveolar space. Additionally, a high dose (500 micrograms/ml) of SSG was needed to activate AMs in vitro. These data imply that the stimulation by SSG alone is not effective on AM activation. SSG administered i.v. also augmented interferon gamma (IFN gamma) mRNA expression in the lung tissue, and the kinetic change of the expression was similar to that of AM activation. Additionally, a synergistic effect of SSG and IFN gamma was observed on AM activation in vitro. It may be possible that IFN gamma produced by pulmonary T cells is one of the important factors for AM activation in vivo by SSG injection. Furthermore, SSG administered i.v. enhanced candidacidal activity and cytolytic activity against pulmonary metastatic Lewis lung carcinoma (3LL) cells of AMs, and inhibited significantly the experimental pulmonary metastasis of 3LL cells. These observations are very useful for the clinical application of SSG as a biological response modifier (BRM).
在本研究中，我们检测了全身性给予SSG（一种从真菌核盘菌IFO 9395中获得的可溶性高度分支的(1→3)-β-D-葡聚糖）对小鼠肺部免疫反应的影响。静脉注射（i.v.）给予的SSG（10 mg/kg）迅速渗漏到肺泡腔中，并在给药后第1天增强了肺泡巨噬细胞（AM）的多种功能，如吞噬活性、溶酶体酶活性、活性氧分泌和细胞因子产生。然而，SSG处理后其流入肺泡的动力学变化和AM激活情况不同。当肺泡腔中仍存在SSG时，AM功能增强在第2天降至对照值。此外，体外激活AM需要高剂量（500微克/毫升）的SSG。这些数据表明，单独用SSG刺激对AM激活无效。静脉注射SSG还增强了肺组织中干扰素γ（IFNγ）mRNA的表达，且该表达的动力学变化与AM激活的变化相似。此外，在体外观察到SSG和IFNγ对AM激活有协同作用。肺T细胞产生的IFNγ可能是静脉注射SSG在体内激活AM的重要因素之一。此外，静脉注射SSG增强了AM对肺部转移性Lewis肺癌（3LL）细胞的杀念珠菌活性和细胞溶解活性，并显著抑制了3LL细胞的实验性肺转移。这些观察结果对于SSG作为生物反应调节剂（BRM）的临床应用非常有用。
