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C57BL/10/CR小鼠:对细菌脂多糖的脂质A部分激活无反应者。

C57BL/10/CR mice: nonresponders to activation by the lipid a moiety of bacterial lipopolysaccharide.

作者信息

McAdam K P, Ryan J L

出版信息

J Immunol. 1978 Jan;120(1):249-53.

PMID:342603
Abstract

C57BL/10/CR mice do not respond to the lipid A moiety of LPS. This defect was demonstrated in vivo by a decreased production of the acute phase serum amyloid protein SAA. In addition, the defect was demonstrated in vitro by using cultures of spleen cells and peritoneal cells. No mitogenesis of spleen cells or enhanced glucose utilization by either spleen cells or peritoneal cells was observed when the cells were stimulated by lipid A or phenol-extracted Escherichia coli K235 LPS. The response of these mice to PHA, Con A, Poly I:C, 8BrcGMP, and butanol extraced E. coli K235 LPS was normal. Thus, the inability of lipid A to stimulate B lymphocyte mitogenesis and activate peritoneal cells in vitro may correlate with its inability to induce the acute phase SAA in vivo. B10/CR mice represent another strain, similar to the C3H/HeJ, which is nonresponsive to lipid A and should be useful in eludcidating the mechanism by which bacterial LPS activates cells.

摘要

C57BL/10/CR小鼠对脂多糖的脂质A部分无反应。这种缺陷在体内表现为急性期血清淀粉样蛋白SAA的产生减少。此外,通过使用脾细胞和腹膜细胞培养物在体外证实了这种缺陷。当细胞受到脂质A或酚提取的大肠杆菌K235脂多糖刺激时,未观察到脾细胞的有丝分裂或脾细胞或腹膜细胞对葡萄糖利用的增强。这些小鼠对PHA、Con A、聚肌胞苷酸、8-溴环鸟苷酸和丁醇提取的大肠杆菌K235脂多糖的反应正常。因此,脂质A在体外无法刺激B淋巴细胞有丝分裂和激活腹膜细胞,这可能与其在体内无法诱导急性期SAA有关。B10/CR小鼠代表了另一种类似于C3H/HeJ的品系,对脂质A无反应,在阐明细菌脂多糖激活细胞的机制方面应会很有用。

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