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首页> 外文期刊>Infection and immunity >Studies on the mechanism of peptidoglycan- and lipopolysaccharide-induced polyclonal activation.
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Studies on the mechanism of peptidoglycan- and lipopolysaccharide-induced polyclonal activation.

机译：肽聚糖和脂多糖诱导的多克隆激活机制的研究。

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Peptidoglycan (PG) and lipopolysaccharide (LPS) are T cell-independent B cell mitogens and polyclonal activators in mice. The mechanism of in vitro proliferation and polyclonal activation of mouse splenocytes induced by PG from Staphylococcus aureus and LPS from Escherichia coli was further studied by using [3H]thymidine incorporation and protein A hemolytic plaque assays. Concanavalin A-generated suppressor cells suppressed both polyclonal and proliferative responses induced by PG, LPS, and pokeweed mitogen. The suppression of the proliferative responses was similar for all these mitogens, but was significantly less pronounced than the suppression of the polyclonal antibody response. Polyclonal activation induced by LPS was the most susceptible to suppression by concanavalin A-generated suppressor cells, and the suppression was significantly greater than in the PG-induced polyclonal response. Also, PG-induced polyclonal activation was not susceptible to inhibition by polymyxin B, which is an inhibitor of other B cell mitogens and polyclonal activators. For optimal generation of immunoglobulin-secreting cells, PG of LPS had to be present for at least 48 h after the initiation of the cultures. Removal of the mitogens after 4 or 24 h of incubation resulted in a suboptimal response. For effective induction of the proliferative response, the mitogens had to be present in cultures for over 24 h. Polyclonal-activating properties of staphylococcal cell wall components were also compared. PG was by far the most potent inducer of polyclonal antibodies. Teichoic acid was not active as a polyclonal activator, whereas purified cell wall and protein A were very weak inducers of polyclonal antibodies. These studies demonstrate that PG, in addition to LPS, can be a useful probe for studies on polyclonal activation.
机译：肽聚糖（PG）和脂多糖（LPS）是小鼠中与T细胞无关的B细胞有丝分裂原和多克隆激活因子。使用[3H]胸苷掺入法和蛋白A溶血噬菌斑试验，进一步研究了金黄色葡萄球菌PG和大肠杆菌LPS诱导的小鼠脾细胞的体外增殖和多克隆激活机制。伴刀豆球蛋白A生成的抑制细胞抑制PG，LPS和商陆有丝分裂原诱导的多克隆和增殖反应。对于所有这些有丝分裂原，增殖反应的抑制是相似的，但远没有多克隆抗体反应的抑制明显。 LPS诱导的多克隆激活最易被伴刀豆球蛋白A产生的抑制细胞抑制，抑制作用明显大于PG诱导的多克隆反应。同样，PG诱导的多克隆激活不易受到多粘菌素B的抑制，多粘菌素B是其他B细胞有丝分裂原和多克隆激活剂的抑制剂。为了最佳地产生分泌免疫球蛋白的细胞，培养开始后，LPS PG必须存在至少48 h。温育4或24小时后去除有丝分裂原导致次优反应。为了有效地诱导增殖反应，在培养物中必须存在有丝分裂原24小时以上。还比较了葡萄球菌细胞壁成分的多克隆激活特性。迄今为止，PG是最有效的多克隆抗体诱导剂。 Teichoic acid没有活性作为多克隆激活剂，而纯化的细胞壁和蛋白A是非常弱的多克隆抗体诱导剂。这些研究表明，除LPS外，PG还可作为研究多克隆激活的有用探针。

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