Schreiber G, Tsykin A, Aldred A R, Thomas T, Fung W P, Dickson P W, Cole T, Birch H, De Jong F A, Milland J
Russell Grimwade School of Biochemistry, University of Melbourne, Parkville, Victoria, Australia.
Ann N Y Acad Sci. 1989;557:61-85; discussion 85-6. doi: 10.1111/j.1749-6632.1989.tb24000.x.
In the rodent, the general response to acute inflammation and tissue damage is characterized by a complex rearrangement in the pattern of concentrations of proteins in the plasma leading to an increase in the sedimentation rate of erythrocytes, an increase in leukocyte concentration in the bloodstream, and a decrease in the hematocrit. Body temperature changes only slightly or not at all. The reasons for the change in plasma concentrations of proteins are changes in their rates of synthesis in the liver. Degradation of plasma proteins is not affected. The details of the acute phase response evolved in the interaction of species with their environment. Therefore, it is not surprising to find differences in the details of the acute phase response among species. For example, alpha 2-macroglobulin is a strongly positive acute phase reactant in the rat, but not in the mouse; C-reactive protein is a strongly positive acute phase protein in the mouse, but is not found in the rat. An inducible acute phase cysteine proteinase inhibitor system, which has evolved from a primordial kininogen gene, has been observed so far only in the rat. The changes in the synthesis rates of acute phase proteins during inflammation are closely reflected by corresponding changes in intracellular mRNA levels. In the liver, the capacity to induce the acute phase pattern of synthesis and secretion of plasma proteins probably develops around birth. Changes in mRNA levels are brought about by changes in transcription rates or by changes in mRNA stability. Kinetics of mRNA changes during the acute phase response differ for individual proteins. The main signal compound for eliciting the acute phase response in liver seems to be interleukin-6/interferon-beta 2/hepatocyte stimulating factor, whereas interleukin-1 leads to typical acute phase changes in mRNA levels only for alpha 1-acid glycoprotein, albumin, and transthyretin. Plasma protein genes are expressed in various extrahepatic tissues, such as the choroid plexus, the yolk sac, the placenta, the seminal vesicles, and other sites. All these tissues are involved in maintaining protein homeostasis in associated extracellular compartments by synthesis and secretion of proteins. Synthesis and secretion of plasma proteins in paracompartmental organs other than the liver is not influenced by the acute phase stimuli.
在啮齿动物中，对急性炎症和组织损伤的一般反应的特征是血浆中蛋白质浓度模式的复杂重排，导致红细胞沉降率增加、血流中白细胞浓度增加以及血细胞比容降低。体温仅有轻微变化或根本没有变化。血浆蛋白质浓度变化的原因是其在肝脏中的合成速率发生了改变。血浆蛋白质的降解未受影响。急性期反应的细节是在物种与环境的相互作用中演变而来的。因此，在不同物种的急性期反应细节中发现差异并不奇怪。例如，α2-巨球蛋白在大鼠中是一种强阳性急性期反应物，但在小鼠中不是；C反应蛋白在小鼠中是一种强阳性急性期蛋白，但在大鼠中未发现。一种从原始激肽原基因进化而来的可诱导急性期半胱氨酸蛋白酶抑制剂系统，迄今为止仅在大鼠中观察到。炎症期间急性期蛋白合成速率的变化密切反映在细胞内mRNA水平的相应变化中。在肝脏中，诱导血浆蛋白合成和分泌急性期模式的能力可能在出生前后发育。mRNA水平的变化是由转录速率的变化或mRNA稳定性的变化引起的。急性期反应期间mRNA变化的动力学因个体蛋白质而异。引发肝脏急性期反应的主要信号化合物似乎是白细胞介素-6/干扰素-β2/肝细胞刺激因子，而白细胞介素-1仅导致α1-酸性糖蛋白、白蛋白和转甲状腺素蛋白的mRNA水平出现典型的急性期变化。血浆蛋白基因在各种肝外组织中表达，如脉络丛、卵黄囊、胎盘、精囊和其他部位。所有这些组织都通过蛋白质的合成和分泌参与维持相关细胞外隔室中的蛋白质稳态。肝脏以外的旁隔室器官中血浆蛋白的合成和分泌不受急性期刺激的影响。
