Reversing the Resistance Phenotype of the Biomphalaria glabrata Snail Host Schistosoma mansoni Infection by Temperature Modulation
Reversing the Resistance Phenotype of the Biomphalaria glabrata Snail Host Schistosoma mansoni Infection by Temperature Modulation
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DOI：
10.1371/journal.ppat.1002677
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发表时间：
2012-04-01
期刊：
影响因子：
6.7
通讯作者：
Knight, Matty
中科院分区：
文献类型：
--
作者：
Ittiprasert, Wannaporn;Knight, Matty
显示对寄生吸虫曼氏血吸虫具有抗性或敏感表型的光滑双脐螺为阐明螺-宿主/寄生虫关系的分子基础提供了宝贵的资源。以前，我们表明，诱导应激基因无论是热休克或寄生虫感染后的一个主要特征区分青少年敏感蜗牛从他们的抗性同行。为了研究热应激和蜗牛易感性之间的这种明显关联，我们研究了温度调制在抗性蜗牛原种BS-90中的作用。在这里，我们表明，在感染前在32摄氏度下孵育长达4小时，这些抗性蜗牛变得对感染易感，即在暴露后5周（PE）脱落尾蚴，而未应激的抗性蜗牛如预期的那样保持抗性。这表明这种抗性蜗牛表型对感染的易感性是温度敏感的（ts）。此外，热应激后用Hsp 90特异性抑制剂格尔德霉素（GA）处理的抗性蜗牛不再对感染敏感，保留了它们的抗性表型。一致地，在寄生虫暴露之前用100 mM GA处理的易感蜗牛表型也保持未感染。这些结果为B中胁迫基因（热休克蛋白; Hsp 70、Hsp 90和Nimbus non-LTR逆转录转座子的逆转录酶[RT]结构域）的诱导提供了直接证据。glabrata对S. mansoni感染，并将抗性BS-90蜗牛表征为温度敏感表型。本研究旨在逆转钉螺对S. mansoni提供了直接追踪构成B基础的分子途径的机会。glabrata蜗牛的能力，无论是维持或破坏S。曼氏寄生虫
Biomphalaria glabrata snails that display either resistant or susceptible phenotypes to the parasitic trematode, Schistosoma mansoni provide an invaluable resource towards elucidating the molecular basis of the snail-host/schistosome relationship. Previously, we showed that induction of stress genes either after heat-shock or parasite infection was a major feature distinguishing juvenile susceptible snails from their resistant counterparts. In order to examine this apparent association between heat stress and snail susceptibility, we investigated the effect of temperature modulation in the resistant snail stock, BS-90. Here, we show that, incubated for up to 4 hrs at 32 degrees C prior to infection, these resistant snails became susceptible to infection, i.e. shedding cercariae at 5 weeks post exposure (PE) while unstressed resistant snails, as expected, remained resistant. This suggests that susceptibility to infection by this resistant snail phenotype is temperature-sensitive (ts). Additionally, resistant snails treated with the Hsp 90 specific inhibitor, geldanamycin (GA) after heat stress, were no longer susceptible to infection, retaining their resistant phenotype. Consistently, susceptible snail phenotypes treated with 100 mM GA before parasite exposure also remained uninfected. These results provide direct evidence for the induction of stress genes (heat shock proteins; Hsp 70, Hsp 90 and the reverse transcriptase [RT] domain of the nimbus non-LTR retrotransposon) in B. glabrata susceptibility to S. mansoni infection and characterize the resistant BS-90 snails as a temperature-sensitive phenotype. This study of reversing snail susceptibility phenotypes to S. mansoni provides an opportunity to directly track molecular pathway(s) that underlie the B. glabrata snail's ability to either sustain or destroy the S. mansoni parasite.