Kaplan R A, Zwiers S H, Yan G
Department of Biological Sciences, State University of New York, Buffalo, New York 14260, USA.
Exp Parasitol. 2001 Jul;98(3):115-22. doi: 10.1006/expr.2001.4623.
Despite significant progress in the identification of the genetic basis of the refractory phenotype, little is known about the physiological mechanism of refractoriness. This study therefore examined the physiological basis of mosquito refractoriness in the Aedes aegypti/P. gallinaceum system, in which a selected refractory strain does not permit Plasmodium oocyst formation. We examined the kinetics of two major proteolytic enzymes involved in blood meal digestion and the dynamics of ookinete formation for two refractory populations (strains Moyo-R and Formosus) and one susceptible population (strain Red). Healthy ookinetes were observed in both the susceptible and the refractory populations, although the susceptible population generally exhibited higher enzymatic activity for trypsin and aminopeptidase than the refractory populations. Parasite numbers in the susceptible Red population showed a 4- to 7-fold decrease in abundance during the transition from the ookinete stage to the oocyst stage, far less than the refractory populations (30- to 92-fold reduction). Due to its smaller body size, Moyo-R individuals generally ingest a smaller blood meal and thus intake fewer gametocytes than Red individuals. Thus, the possibility that refractoriness in the Moyo-R population results from fewer gametocytes being ingested is examined. We found that the Red population remained highly susceptible and the Moyo-R population stayed refractory when those individuals with similar blood meal size were compared. We conclude that failure of oocyst development in the refractory mosquitoes is not due to ookinete damage by proteolytic enzymes or to fewer gametocytes being ingested, but rather is due to a midgut barrier or to some other mechanism.
尽管在确定难治性表型的遗传基础方面取得了重大进展，但对难治性的生理机制却知之甚少。因此，本研究在埃及伊蚊/鸡疟原虫系统中研究了蚊子难治性的生理基础，在该系统中，一个选定的难治性品系不允许疟原虫卵囊形成。我们研究了参与血餐消化的两种主要蛋白水解酶的动力学以及两个难治性种群（莫约-R品系和福尔摩索斯品系）和一个易感种群（红品系）的动合子形成动态。在易感种群和难治性种群中均观察到了健康的动合子，尽管易感种群的胰蛋白酶和氨肽酶酶活性通常高于难治性种群。在从动合子阶段到卵囊阶段的转变过程中，易感红种群中的寄生虫数量丰度下降了4至7倍，远低于难治性种群（减少30至92倍）。由于莫约-R个体体型较小，它们通常摄取的血餐较小，因此摄入的配子体比红个体少。因此，研究了莫约-R种群的难治性是否是由于摄入的配子体较少所致。我们发现，当比较血餐量相似的个体时，红种群仍然高度易感，而莫约-R种群仍然难治。我们得出结论，难治性蚊子中卵囊发育失败不是由于蛋白水解酶对动合子的破坏或摄入的配子体较少，而是由于中肠屏障或某种其他机制。
