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急性营养缺乏对小鼠免疫功能的影响。I. 巨噬细胞。

Effect of acute nutritional deprivation on immune function in mice. I. Macrophages.

作者信息

Wing E J, Barczynski L K, Boehmer S M

出版信息

Immunology. 1983 Mar;48(3):543-50.

Abstract

This study was designed to explore the effects of acute nutritional deprivation (starvation) on macrophage function in mice. In vivo macrophage activity was increased by starvation, as determined by multiplication of Listeria monocytogenes in both spleens and livers after intravenous injection. Similarly, in vitro studies revealed that the capacity of peritoneal macrophages to kill listeria was enhanced by starvation. This function was increased further by the addition of small concentrations of lipopolysaccharide (LPS; 10-100 ng/ml). The bactericidal activity of macrophages from starved mice, however, did not reach the levels observed with macrophages from BCG-infected mice. Furthermore, LPS did not appear to be an important second signal for macrophage activation in vivo, as LPS-unresponsive mice (C3H/HeJ and A/J) were protected by starvation. In contrast to these results we found that starved mice were not protected against Toxoplasma gondii infection and that macrophages from starved mice were unable to prevent multiplication of toxoplasma trophozoites in vitro. In toto, these experiments suggest that macrophage function is enhanced by starvation, but that this enhancement is not sufficient to fulfill all criteria for macrophage activation.

摘要

本研究旨在探讨急性营养缺乏(饥饿)对小鼠巨噬细胞功能的影响。静脉注射后,通过脾脏和肝脏中单核细胞增生李斯特菌的繁殖情况测定,饥饿可使体内巨噬细胞活性增强。同样,体外研究表明,饥饿可增强腹腔巨噬细胞杀灭李斯特菌的能力。添加低浓度脂多糖(LPS;10 - 100 ng/ml)可进一步增强该功能。然而,饥饿小鼠巨噬细胞的杀菌活性未达到卡介苗感染小鼠巨噬细胞所观察到的水平。此外,LPS似乎并非体内巨噬细胞激活的重要第二信号,因为对LPS无反应的小鼠(C3H/HeJ和A/J)受到饥饿的保护。与这些结果相反,我们发现饥饿小鼠无法抵御刚地弓形虫感染,且饥饿小鼠的巨噬细胞在体外无法阻止弓形虫滋养体的繁殖。总体而言,这些实验表明饥饿可增强巨噬细胞功能,但这种增强不足以满足巨噬细胞激活的所有标准。

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Role of nutrition in immunologic function.营养在免疫功能中的作用。
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