Prioli R P, Rosenberg I, Pereira M E
New England Medical Center Hospitals, Dept. of Geographic Medicine and Infectious Diseases, Boston, MA 02111.
Mol Biochem Parasitol. 1990 Jan 15;38(2):191-8. doi: 10.1016/0166-6851(90)90022-e.
Trypanosoma cruzi exhibits a developmentally regulated neuraminidase activity that is inhibited by high-density lipoprotein (HDL). We report here that the infection of culture cells by T. cruzi trypomastigotes is enhanced by HDL in a dose-dependent manner. The enhanced infection is prevented by Vibrio cholerae neuraminidase, an enzyme whose activity is not inhibited by HDL, suggesting that sialic acid is involved in T. cruzi-host interaction. Similar enhancement of infection is also produced by low-density lipoprotein (LDL), which inhibits T. cruzi neuraminidase as well as HDL. Further evidence that the enhancement is due to lipoproteins is provided by the fact that infection of host cells in lipoprotein-deficient medium is less than in normal medium; it can be restored to the higher level by the addition of HDL, LDL or both to the lipoprotein-deficient medium. In view of these results, we propose that HDL and LDL regulate T. cruzi infection in mammalian hosts by inhibiting the parasite neuraminidase activity.
克氏锥虫表现出一种受发育调控的神经氨酸酶活性，该活性受到高密度脂蛋白（HDL）的抑制。我们在此报告，HDL以剂量依赖的方式增强了克氏锥虫滋养体对培养细胞的感染。霍乱弧菌神经氨酸酶可阻止这种增强的感染，该酶的活性不受HDL抑制，这表明唾液酸参与了克氏锥虫与宿主的相互作用。低密度脂蛋白（LDL）也能产生类似的感染增强作用，它与HDL一样能抑制克氏锥虫神经氨酸酶。脂蛋白缺乏培养基中宿主细胞的感染少于正常培养基，这一事实进一步证明了这种增强作用是由脂蛋白引起的；向脂蛋白缺乏培养基中添加HDL、LDL或两者，可将感染恢复到更高水平。鉴于这些结果，我们提出HDL和LDL通过抑制寄生虫神经氨酸酶活性来调节哺乳动物宿主中的克氏锥虫感染。
