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首页> 外文期刊>Microbes and infection >Response of rat fasciculata-reticularis cells in primary culture to bacterial lipopolysaccharide.
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Response of rat fasciculata-reticularis cells in primary culture to bacterial lipopolysaccharide.

机译：原代培养中的大鼠束状网状细胞对细菌脂多糖的反应。

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The aim of this study was to determine the direct effect of a wide range of concentrations of lipopolysaccharide (LPS) of Escherichia coli O111:B4 on fasciculata-reticularis cells in primary cultures. In short-term cultures of fasciculata-reticularis cells, the presence of low (1-10 microg/ml) doses of LPS in the medium produced a decrease in ACTH-induced corticosterone secretion, in a dose-dependent manner and independent of the culture medium. The corticosterone production stimulated by db-cAMP was slightly decreased by the presence of LPS in culture medium, while the pregnenolone induced corticosterone biosynthesis was not modified. LPS modified the binding of [125I]-Tyr23-ACTH to the fasciculata-reticularis cell membrane and the signal transduction pathway, as LPS reduced ACTH-induced cAMP production. In long-term cultures, the presence of LPS in the medium produces a decrease in the specific binding of [125I]-Tyr23-ACTH, while the presence of ACTH in the culture medium produced an increase in its specific binding. The use of high doses of LPS (100-250 microg/ml) has helped to clarify some aspects of the LPS action. These doses of LPS severely inhibited ACTH-induced corticosterone production, and clearly reduced the corticosterone production stimulated by db-cAMP and the binding of ACTH to its receptors. In long-term cultures, LPS decreased the number of ACTH receptors, an effect that was reversed by subsequent exposure to ACTH. These results indicate that LPS exerts a direct action on fasciculata-reticularis cells and a model of the mechanism of LPS action is proposed.
机译：这项研究的目的是确定大范围浓度的大肠杆菌O111：B4脂多糖（LPS）对原代培养的网状筋膜细胞的直接影响。在Fasciculata-reticularis细胞的短期培养中，培养基中低剂量（1-10 microg / ml）LPS的存在以剂量依赖的方式独立于培养物，导致ACTH诱导的皮质酮分泌减少中。培养基中存在LPS，db-cAMP刺激的皮质酮产量略有降低，而孕烯醇酮诱导的皮质酮生物合成未改变。 LPS修饰了[125I] -Tyr23-ACTH与束状网状细胞膜和信号转导途径的结合，因为LPS减少了ACTH诱导的cAMP产生。在长期培养中，培养基中LPS的存在会降低[125I] -Tyr23-ACTH的特异性结合，而培养基中ACTH的存在会导致其特异性结合增加。使用大剂量的LPS（100-250 microg / ml）有助于阐明LPS作用的某些方面。这些剂量的LPS严重抑制了ACTH诱导的皮质酮生成，并明显降低了db-cAMP刺激的ACTH与其受体结合的皮质酮生成。在长期培养中，LPS减少了ACTH受体的数量，这种作用随后被ACTH所逆转。这些结果表明，LPS对网状筋膜细胞具有直接作用，并提出了LPS作用机理的模型。

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