ROWLEY D
J Exp Med. 1960 Jan 1;111(1):137-44. doi: 10.1084/jem.111.1.137.
A study of the recoveries of radioactivity, and of viable bacteria following injection of P(32)-labelled E. coli into the mouse peritoneum, has indicated that the rapid decrease in viable bacteria which occurs is largely due to peritoneal events, and not to the transport of bacteria elsewhere. The serum from mice given lipopolysaccharides 48 hours previously, when used to pretreat bacteria before intraperitoneal injection, was found to stimulate phagocytosis to a greater extent than did pretreatment with normal serum. In addition, macrophages themselves were found to be affected by contact with lipopolysaccharides, either in vivo or in vitro in such a way as to promote their phagocytic abilities. It is suggested that the provocation of non-specific immunity by bacterial lipopolysaccharides involves two facets at least; firstly, an increase in the opsonic capacity of the serum, and secondly an increase in the inherent capacity of phagocytic cells to perform this function.
一项关于将P(32)标记的大肠杆菌注入小鼠腹腔后放射性物质和活菌恢复情况的研究表明,活菌数量的快速减少主要是由于腹腔内的事件,而非细菌向其他部位的转移。发现给小鼠注射脂多糖48小时后的血清,在腹腔注射前用于预处理细菌时,比用正常血清预处理能更大程度地刺激吞噬作用。此外,发现巨噬细胞自身无论是在体内还是体外与脂多糖接触后,其吞噬能力都会受到影响,从而得到促进。有人提出,细菌脂多糖激发非特异性免疫至少涉及两个方面:首先,血清调理素能力的增强;其次,吞噬细胞执行该功能的内在能力的增强。