Leishmania donovani parasites are the cause of visceral leishmaniasis and are transmitted by bites from phlebotomine sand flies. A prominent feature of vector-transmitted Leishmania is the persistence of neutrophils at bite sites, where they protect captured parasites, leading to enhanced disease. Here, we demonstrate that gut microbes from the sand fly are egested into host skin alongside Leishmania parasites. The egested microbes trigger the inflammasome, leading to a rapid production of interleukin-1β (IL-1β), which sustains neutrophil infiltration. Reducing midgut microbiota by pretreatment of Leishmania-infected sand flies with antibiotics or neutralizing the effect of IL-1β in bitten mice abrogates neutrophil recruitment. These early events are associated with impairment of parasite visceralization, indicating that both gut microbiota and IL-1β are important for the establishment of Leishmania infections. Considering that arthropods harbor a rich microbiota, its potential egestion after bites may be a shared mechanism that contributes to severity of vector-borne disease.

利什曼原虫donovani寄生虫是内脏利什曼原虫病的病因，并通过le蛇毒sand的叮咬传播。媒介传播的利什曼原虫的一个显着特征是嗜中性粒细胞在叮咬部位的持久性，它们在这里保护捕获的寄生虫，从而导致疾病加剧。在这里，我们证明了沙蝇中的肠道微生物与利什曼原虫寄生虫一起进入宿主皮肤。病原微生物触发炎症小体，导致白细胞介素-1β（IL-1β）快速产生，维持中性粒细胞浸润。利什曼原虫预处理减少中肠微生物群被抗生素感染的沙蝇或叮咬小鼠中和IL-1β的作用会废除嗜中性白细胞。这些早期事件与寄生虫内脏损伤有关，表明肠道菌群和IL-1β对建立利什曼原虫感染很重要。考虑到节肢动物具有丰富的微生物群，被咬后潜在的节食可能是导致媒介传播疾病严重程度的共同机制。