Tunaz Hasan, Park Youngjin, Büyükgüzel Kemal, Bedick Jon C, Nor Aliza A R, Stanley David W
Insect Biochemical Physiology Laboratory, University of Nebraska, Lincoln 68583-0816, USA.
Arch Insect Biochem Physiol. 2003 Jan;52(1):1-6. doi: 10.1002/arch.10056.
Intracellular phospholipase A(2) (PLA(2)) is responsible for releasing arachidonic acid from cellular phospholipids, and is thought to be the first step in eicosanoid biosynthesis. Intracellular PLA(2)s have been characterized in fat body and hemocytes from tobacco hornworms, Manduca sexta. Here we show that bacterial challenge stimulated increased PLA(2) activity in isolated hemocyte preparations, relative to control hemocyte preparations that were challenged with water. The increased activity was detected as early as 15 s post-challenge and lasted for at least 1 h. The increased activity depended on a minimum bacterial challenge dose, and was inhibited in reactions conducted in the presence of oleyoxyethylphosphorylcholine, a site-specific PLA(2) inhibitor. In independent experiments with serum prepared from whole hemolymph, we found no PLA(2) activity was secreted into serum during the first 24 h following bacterial infection. We infer that a hemocytic intracellular PLA(2) activity is increased immediately an infection is detected. The significance of this enzyme lies in its role in launching the biosynthesis of eicosanoids, which mediate cellular immune reactions to bacterial infection.
细胞内磷脂酶A2（PLA2）负责从细胞磷脂中释放花生四烯酸，被认为是类花生酸生物合成的第一步。在烟草天蛾曼陀罗的脂肪体和血细胞中已对细胞内PLA2进行了表征。在此我们表明，相对于用水处理的对照血细胞制剂，细菌刺激会使分离的血细胞制剂中的PLA2活性增加。这种活性增加在刺激后15秒就被检测到，并持续至少1小时。活性增加取决于最小细菌刺激剂量，并且在存在位点特异性PLA2抑制剂油酰氧乙基磷酰胆碱的反应中受到抑制。在使用从全血淋巴制备的血清进行的独立实验中，我们发现在细菌感染后的最初24小时内，没有PLA2活性分泌到血清中。我们推断，一旦检测到感染，血细胞内PLA2活性就会立即增加。这种酶的重要性在于其在启动类花生酸生物合成中的作用，类花生酸介导对细菌感染的细胞免疫反应。
