Filkins J P
Fed Proc. 1985 Feb;44(2):300-4.
The role of the macrophage system in shock pathogenesis now embraces both classic endocytic functions as well as the more recently discovered function of the macrophages as a multifaceted secretory apparatus. Among the major macrophage secretory products are the monokines, regulatory proteins that mediate via both local or paracrine and systemic or endocrine mechanisms, the nonspecific host defense and metabolic responses to inflammation and sepsis. Evidence is reviewed for a monokine involvement in the alterations of protein, fat, and carbohydrate metabolism in sepsis and/or endotoxicosis, viz., enhanced muscle proteolysis, enhanced hepatic acute phase protein synthesis, depressed lipogenesis and lipoprotein lipase function, enhanced peripheral glucose oxidation, and depression of hepatic gluconeogenesis. Monokines are also related to the disturbed endocrine mechanisms of sepsis, viz., enhanced insulin secretion and depressed adrenal steroidogenesis. It is suggested that the macrophage system mediates via secretion of monokines an integrated fuel substrate and hormonal adjustment to sepsis, which on the one hand may provide optimal metabolic homeostasis for systemic host defense, but on the other hand, if allowed to act unchecked, may contribute to the metabolic dyshomeostasis of septic shock.
巨噬细胞系统在休克发病机制中的作用，如今既涵盖了经典的内吞功能，也包括巨噬细胞作为多面分泌器官这一最近才发现的功能。巨噬细胞的主要分泌产物包括单核因子，即通过局部或旁分泌以及全身或内分泌机制介导非特异性宿主防御以及对炎症和脓毒症的代谢反应的调节蛋白。本文综述了单核因子参与脓毒症和/或内毒素血症中蛋白质、脂肪和碳水化合物代谢改变的证据，即增强肌肉蛋白水解、增强肝脏急性期蛋白合成、抑制脂肪生成和脂蛋白脂肪酶功能、增强外周葡萄糖氧化以及抑制肝脏糖异生。单核因子还与脓毒症紊乱的内分泌机制有关，即增强胰岛素分泌和抑制肾上腺类固醇生成。有人提出，巨噬细胞系统通过分泌单核因子介导对脓毒症的综合燃料底物和激素调节，这一方面可为全身宿主防御提供最佳的代谢稳态，但另一方面，如果不受控制地发挥作用，可能会导致脓毒性休克的代谢失调。
