Tayek J A, Blackburn G L
Am J Med. 1984 May 15;76(5A):81-90. doi: 10.1016/0002-9343(84)90248-1.
Defense mechanisms employed by the host to fight infection are highly dependent on adequate protein synthesis to support phagocytic and lymphoid cell activity as well as immunoglobulin production. Interleukin I is a small, not yet fully characterized protein produced by macrophages which appears to initiate most of the nonspecific metabolic changes observed during infection. These alterations include: increase in the synthesis of visceral proteins, white blood cells, and acute phase globulins; enhanced somatic protein breakdown; sequestering of serum iron and zinc in the liver; and induction of fever. The ability of leukocytes to produce interleukin I is impaired in patients with visceral protein depletion or kwashiorkor-like, hypoalbuminemic malnutrition and can be restored in the healthy unstressed patient within approximately three to five days by feeding. Similarly, in the stressed patient, adequate protein and caloric intake improves the ability to produce interleukin I, which may improve survival. Other defects in host defense in advanced stages of protein malnutrition include lymphopenia, impaired phagocytosis, and deficiencies in fibronectin, immunoglobulins, and complement levels. Thus, the goal of nutritional support is to maintain sufficient amounts of amino acids for visceral protein synthesis required for adequate host defense.
宿主对抗感染所采用的防御机制高度依赖于充足的蛋白质合成，以支持吞噬细胞和淋巴细胞的活性以及免疫球蛋白的产生。白细胞介素I是一种由巨噬细胞产生的小分子蛋白质，其特性尚未完全明确，它似乎引发了感染期间观察到的大多数非特异性代谢变化。这些变化包括：内脏蛋白、白细胞和急性期球蛋白合成增加；体细胞蛋白分解增强；肝脏中血清铁和锌的螯合；以及发热的诱导。在内脏蛋白缺乏或类似夸希奥科病的低白蛋白血症性营养不良患者中，白细胞产生白细胞介素I的能力受损，通过喂养，健康且未受应激的患者在大约三到五天内这种能力可恢复。同样，在应激患者中，充足的蛋白质和热量摄入可提高产生白细胞介素I的能力，这可能会提高生存率。蛋白质营养不良晚期宿主防御的其他缺陷包括淋巴细胞减少、吞噬作用受损以及纤连蛋白、免疫球蛋白和补体水平缺乏。因此，营养支持的目标是维持足够量的氨基酸，用于宿主进行充分防御所需的内脏蛋白合成。
