Keusch G T, Douglas S D, Hammer G, Braden K
J Infect Dis. 1978 Aug;138(2):134-42. doi: 10.1093/infdis/138.2.134.
Cellular and humoral aspects of the antibacterial activity of macrophages during experimental protein-calorie malnutrition were studied. There were no defects in chemotaxis or bactericidal activity of cells from protein-deficient animals, although phagocytosis-associated oxygen consumption and hexose monophosphate shunt activity were depressed. However, marked impairment of humoral chemotactic factors generated in the peritoneal cavity by glycogen injection and of heatlabile serum opsonins for Staphylococcus aureus, Escherichia coli, Salmonella typhimurium, and Salmonella enteritidis was found. The studies suggested that some macrophage antibacterial functions measured in vitro are not altered in experimental acute protein-calorie malnutrition, but that serum factors, presumably complement-derived, would limit their in vivo function. Thymic involution and lymphocyte depletion would further impair in vivo cellular immune reactions affected by macrophages. This model may therefore prove useful for the study of specific aspects of cellular immunity in malnourished hosts and of specific rehabilitation strategies.
研究了实验性蛋白质 - 热量营养不良期间巨噬细胞抗菌活性的细胞和体液方面。蛋白质缺乏动物的细胞趋化性或杀菌活性没有缺陷,尽管吞噬作用相关的氧消耗和磷酸己糖旁路活性降低。然而,发现通过注射糖原在腹腔中产生的体液趋化因子以及针对金黄色葡萄球菌、大肠杆菌、鼠伤寒沙门氏菌和肠炎沙门氏菌的热不稳定血清调理素明显受损。研究表明,在实验性急性蛋白质 - 热量营养不良中,体外测量的一些巨噬细胞抗菌功能没有改变,但血清因子,可能是补体衍生的,会限制它们的体内功能。胸腺萎缩和淋巴细胞减少会进一步损害受巨噬细胞影响的体内细胞免疫反应。因此,该模型可能被证明对研究营养不良宿主中细胞免疫的特定方面以及特定的康复策略有用。