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暴露于10摄氏度和23摄氏度环境下的小鼠在初次和二次感染沙门氏菌后的比较动力学

Comparative dynamics of salmonella infection after primary and secondary challenge of mice exposed to 10 and 23 C.

作者信息

Previte J J, Alden J C, Egbert M

出版信息

Infect Immun. 1973 Oct;8(4):597-603. doi: 10.1128/iai.8.4.597-603.1973.

Abstract

Mortality of mice increased significantly as a result of cold exposure when the animals were challenged orally with Salmonella typhimurium, strain RIA. As reported earlier, cold exposure alone did not kill control animals nor did oral challenge at room temperature. No differences were apparent in the number of Salmonella per gram of liver-spleen, colon, or lung between groups of infected mice housed at 23 and 10 C. The number of bacteria increased equally in liver-spleen samples during the period of increasing mortality in the group housed at 10 C and the period of overt illness in those housed at 23 C. The ability to clear the bloodstream of a secondary intravenous challenge did not seem to be impaired by cold exposure. The bacterial load in the spleen and the rate of change in weight of that organ was equal in animals given a secondary challenge at 10 or 23 C. However, the absolute spleen weight was less in the cold-exposed group as was survival when the secondary challenge was administered 3 days after the primary oral challenge. The studies indicate that endotoxin from S. typhimurium may sensitize mice to the lethal effects of cold exposure. The increase in mortality observed in cold-exposed, infected mice is not due to greater bacterial proliferation in these animals. Rather, the combined stress effects of the bacterial agent(s) and cold may link lympholytic effects to impaired detoxification and increased energy demands, which often leads to lethal vascular collapse in cold-exposed, infected mice.

摘要

当用鼠伤寒沙门氏菌RIA菌株经口攻击小鼠时,冷暴露会显著增加小鼠的死亡率。如先前报道,单独的冷暴露不会杀死对照动物,在室温下经口攻击也不会。在23℃和10℃饲养的感染小鼠组之间,每克肝脾、结肠或肺中的沙门氏菌数量没有明显差异。在10℃饲养组死亡率增加期间以及23℃饲养组明显发病期间,肝脾样本中的细菌数量同样增加。冷暴露似乎并未损害清除二次静脉注射攻击后血液中细菌的能力。在10℃或23℃接受二次攻击的动物中,脾脏中的细菌载量以及该器官重量的变化率是相等的。然而,冷暴露组的绝对脾脏重量较小,在初次经口攻击3天后进行二次攻击时,其存活率也较低。这些研究表明,鼠伤寒沙门氏菌的内毒素可能使小鼠对冷暴露的致死作用敏感。在冷暴露的感染小鼠中观察到的死亡率增加并非由于这些动物中细菌的大量增殖。相反,细菌因子和寒冷的联合应激效应可能将淋巴细胞溶解作用与解毒受损和能量需求增加联系起来,这通常会导致冷暴露的感染小鼠出现致命性血管崩溃。

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