The mosquito Anopheles stephensi limits malaria parasite development with inducible synthesis of nitric oxide
The mosquito Anopheles stephensi limits malaria parasite development with inducible synthesis of nitric oxide
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DOI：
10.1073/pnas.95.10.5700
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发表时间：
1998-05-12
影响因子：
11.1
通讯作者：
Rosenberg, R
中科院分区：
文献类型：
--
作者：
Luckhart, S;Vodovotz, Y;Rosenberg, R
我们发现斯氏按蚊是人类疟疾的天然媒介，它通过诱导一氧化氮（NO）的合成、A.在疟原虫侵入中肠后不久，在中肠和尸体中检测到与特征性NOS基因高度同源的stephensi NO合酶（NOS）。后来，A。stephensi NOS的表达和酶活性发生在子孢子释放的开始。循环水平的亚硝酸盐/硝酸盐，NO合成的最终产品，显着较高的疟原虫感染的蚊子。饮食中提供NOS底物L-精氨酸减少了A.史蒂芬西与此相反，饮食中提供的NOS抑制剂显着增加寄生虫的数量在受感染的蚊子，证实了A。stephensi限制疟原虫发展与NO。
We have discovered that the mosquito Anopheles stephensi, a natural vector of human malaria, limits parasite development with inducible synthesis of nitric oxide (NO), Elevated expression of A. stephensi NO synthase (NOS), which is highly homologous to characterized NOS genes, was detected in the midgut and carcass soon after invasion of the midgut by Plasmodium, Early induction is likely primed by bacterial growth in the blood meal. Later increases in A. stephensi NOS expression and enzyme activity occurred at the beginning of sporozoite release. Circulating levels of nitrite/nitrate, end-products of NO synthesis, were significantly higher in Plasmodium-infected mosquitoes. Dietary provision of the NOS substrate L-arginine reduced Plasmodium infections in A. stephensi. In contrast, dietary provision of a NOS inhibitor significantly increased parasite numbers in infected mosquitoes, confirming that A. stephensi limits Plasmodium development with NO.