Oka Hideki, Tabara Akiko, Fujisawa Kohei, Jinnai Michio, Nakajima Rui, Arai Satoru, Ishihara Chiaki, Tsuji Masayoshi
School of Veterinary Medicine, Rakuno-Gakuen University, Ebetsu, Hokkaido 069-8501, Japan.
Exp Parasitol. 2008 Nov;120(3):290-4. doi: 10.1016/j.exppara.2008.08.008. Epub 2008 Aug 28.
Despite the evidence suggesting that mouse pyruvate kinase (PK) deficiency provides protection against malaria in rodents, there has been no investigation of a parallel protective effect against babesiosis caused by Babesia rodhaini. Here, we examined whether a PK-deficient co-isogenic mouse strain (CBA-Pk-1(slc)) was protected against B. rodhaini infection. We demonstrated that deficiency in pyruvate kinase correlated with a significant protective effect, with survival rates of 50%, 58% and 56% in groups inoculated with 10, 10(3) and 10(5) parasitized erythrocytes, respectively. In contrast, control CBA (CBA-Pk-1(+)) mice exhibited 100% lethality, regardless of the infectious dose. In addition, CBA-Pk-1(slc) mice showed decreased levels of parasitemia when compared to CBA-Pk-1(+) mice, in groups given 10, 10(3) or 10(5) parasitized erythrocytes. These results indicate that similar to PK deficiency in rodents, PK deficiency in mice affects the in vivo growth of B. rodhaini and protects the mice from lethal babesiosis.
尽管有证据表明小鼠丙酮酸激酶（PK）缺乏可使啮齿动物对疟疾产生抗性，但尚未有人研究其对罗得西亚巴贝斯虫引起的巴贝斯虫病是否具有类似的保护作用。在此，我们研究了PK缺陷同基因小鼠品系（CBA-Pk-1(slc)）是否对罗得西亚巴贝斯虫感染具有抗性。我们发现，丙酮酸激酶缺乏与显著的保护作用相关，接种10、10³和10⁵个感染红细胞的组的存活率分别为50%、58%和56%。相比之下，对照CBA（CBA-Pk-1(+)）小鼠无论感染剂量如何，死亡率均为100%。此外，在给予10、10³或10⁵个感染红细胞的组中，与CBA-Pk-1(+)小鼠相比，CBA-Pk-1(slc)小鼠的寄生虫血症水平较低。这些结果表明，与啮齿动物中的PK缺乏类似，小鼠中的PK缺乏会影响罗得西亚巴贝斯虫在体内的生长，并保护小鼠免受致命的巴贝斯虫病感染。
