Planorbid freshwater snails are important intermediate hosts for parasitic diseases caused by parasitic worms, most notably schistosomiasis. There are numerous reports of snails, specifically Biomphalaria glabrata, having compromised defences against schistosomes after being exposed to thermal stress. Environmental modifications to the defenses of schistosome transmitting snails could have negative ramifications for human disease risk in the context of climate change. Here the effects of heat shock on the production of hydrogen peroxide, a primary anti-microbial effector in many molluscs, were examined. The present findings show that heat shock increases NADPH oxidase 2 mRNA levels and hydrogen peroxide produced by snail hemocytes, and that both of these phenotypes could be reversed by an HSP-90 inhibitor. These findings indicate that snail defense systems are altered by heat shock at a molecular level in B. glabrata, and that snail immunity to many pathogens may be altered by the rapid variations in temperature that are associated with global climate change.

Planorbid 淡水蜗牛是寄生虫引起的寄生虫病的重要中间宿主，最显着的是血吸虫病。有许多关于蜗牛的报道，特别是Biophalaria glabrata，暴露于热应力后，对血吸虫的防御能力受损。在气候变化的背景下，对血吸虫传播蜗牛防御的环境改变可能会对人类疾病风险产生负面影响。在这里，研究了热休克对过氧化氢产生的影响，过氧化氢是许多软体动物的主要抗微生物效应物。目前的研究结果表明，热休克会增加蜗牛血细胞产生的 NADPH 氧化酶 2 mRNA 水平和过氧化氢，并且这两种表型都可以被 HSP-90 抑制剂逆转。这些发现表明蜗牛防御系统在B. glabrata 中被分子水平的热休克改变，而且与全球气候变化相关的温度的快速变化可能会改变蜗牛对许多病原体的免疫力。