Trypanosoma rangeli is the second most common American trypanosome that infects man. It is vectored by triatomines from the genus Rhodnius, in which it invades the hemolymph and infects the salivary glands, avoiding the bug immune responses. In insects, these responses are initiated by well conserved pathways, mainly the IMD, Toll, and Jak/STAT. We hypothesize that long-term infection with T. rangeli in the gut or hemolymph of Rhodnius prolixus triggers different systemic immune responses, which influence the number of parasites that survive inside the vector. Thus, we investigated groups of insects with infections in the gut and/or hemolymph, and evaluated the parasite load and the expression in the fat body of transcription factors (Rp-Relish, Rp-Dorsal, and Rp-STAT) and inhibitors (Rp-Cactus and Rp-Caspar) of the IMD, Toll, and Jak/STAT pathways. We detected lower parasite counts in the gut of insects without hemolymph infection, compared to hemolymph-infected groups. Besides, we measured higher parasite numbers in the gut of bugs that were first inoculated with T. rangeli and then fed on infected mice, compared with control insects, indicating that hemolymph infection increases parasite numbers in the gut. Interestingly, we observed that genes from the three immune pathways where differentially modulated, depending on the region parasites were present, as we found (1) Rp-Relish downregulated in gut-and/or-hemolymph-infected insects, compared with controls; (2) Rp-Cactus upregulated in gut-infected insect, compared with controls and gut-and-hemolymph-infected groups; and (3) Rp-STAT downregulated in all groups of hemolymph-infected insects. Finally, we uncovered negative correlations between parasite loads in the gut and Rp-Relish and Rp-Cactus expression, and between parasite counts in the hemolymph and Rp-Relish levels, suggesting an association between parasite numbers and the IMD and Toll pathways. Overall, our findings reveal new players in R. prolixus–T. rangeli interactions that could be key for the capacity of the bug to transmit the pathogen.

兰氏锥虫是感染人类的​​第二大美国锥虫。它是由属中的三角藻类载体罗得尼乌斯，它会侵入血淋巴并感染唾液腺，从而避免了虫子的免疫反应。在昆虫中，这些反应是由保存良好的途径（主要是IMD，Toll和Jak / STAT）引发的。我们假设长期感染T.兰格里 在肠或血淋巴中 罗氏红景天触发不同的全身免疫反应，从而影响在载体内存活的寄生虫数量。因此，我们调查了在肠道和/或淋巴中有感染的昆虫群，并评估了寄生虫负荷和转录因子在脂肪体内的表达（RP-津津有味， 背背和 统计值）和抑制剂（Rp仙人掌 和 卡斯帕），IMD，收费和Jak / STAT路径。与经血淋巴感染的组相比，我们在未经血淋巴感染的昆虫肠道中检出的寄生虫数量更低。此外，我们在最初接种过的虫子肠道中测出了更高的寄生虫数量T.兰格里然后与对照昆虫相比，以受感染的小鼠为食，表明血淋巴感染会增加肠道中的寄生虫数量。有趣的是，我们发现来自三个免疫途径的基因受到不同的调节，这取决于存在的区域寄生虫，如我们发现的（1）RP-津津有味与对照组相比，肠道和/或血淋巴感染的昆虫表达下调；（2）Rp仙人掌与对照组和肠道和淋巴感染组相比，肠道感染的昆虫中的表达上调；和（3）统计值在所有经血淋巴感染的昆虫中下调。最后，我们发现了肠道中的寄生虫负荷与RP-津津有味 和 Rp仙人掌 表达，以及血淋巴中的寄生虫计数和 RP-津津有味水平，表明寄生虫数量与IMD和Toll通路之间存在关联。总体而言，我们的发现揭示了pro–T.兰格里 交互可能是bug传播病原体能力的关键。