Department of Biological Sciences, Vanderbilt University, Nashville, TN 37235, USA.
Department of Biological Sciences, Vanderbilt University, Nashville, TN 37235, USA
J Exp Biol. 2020 Aug 13;223(Pt 15):jeb225821. doi: 10.1242/jeb.225821.
The circulatory and immune systems of mosquitoes are functionally integrated. An infection induces the migration of hemocytes to the dorsal vessel, and specifically, to the regions surrounding the ostia of the heart. These periostial hemocytes phagocytose pathogens in the areas of the hemocoel that experience the highest hemolymph flow. Here, we investigated whether a bacterial infection affects cardiac rhythmicity in the African malaria mosquito, We discovered that infection with , and , but not , reduces the mosquito heart rate and alters the proportional directionality of heart contractions. Infection does not alter the expression of genes encoding crustacean cardioactive peptide (CCAP), FMRFamide, corazonin, neuropeptide F or short neuropeptide F, indicating that they do not drive the cardiac phenotype. Infection upregulates the transcription of two superoxide dismutase (SOD) genes, catalase and a glutathione peroxidase, but dramatically induces upregulation of nitric oxide synthase (NOS) in both the heart and hemocytes. Within the heart, nitric oxide synthase is produced by periostial hemocytes, and chemically inhibiting the production of nitric oxide using l-NAME reverses the infection-induced cardiac phenotype. Finally, infection induces the upregulation of two lysozyme genes in the heart and other tissues, and treating mosquitoes with lysozyme reduces the heart rate in a manner reminiscent of the infection phenotype. These data demonstrate an exciting new facet of the integration between the immune and circulatory systems of insects, whereby a hemocyte-produced factor with immune activity, namely nitric oxide, modulates heart physiology.
蚊子的循环系统和免疫系统在功能上是整合在一起的。感染会诱导血淋巴细胞迁移到背血管，特别是迁移到心脏口周围的区域。这些周皮血淋巴细胞在经历最高血淋巴流动的血腔区域吞噬病原体。在这里，我们研究了细菌感染是否会影响非洲疟蚊的心脏节律。我们发现，感染 、 和 但不是 会降低蚊子的心率，并改变心脏收缩的比例方向。感染不会改变编码甲壳动物心脏活性肽（CCAP）、FMRFamide、心激素、神经肽 F 或短神经肽 F 的基因的表达，表明它们不会驱动心脏表型。感染上调两种超氧化物歧化酶（SOD）基因、过氧化氢酶和谷胱甘肽过氧化物酶的转录，但在心脏和血淋巴细胞中显著诱导一氧化氮合酶（NOS）的上调。在心脏中，一氧化氮合酶由周皮血淋巴细胞产生，用 l-NAME 抑制一氧化氮的产生可逆转感染引起的心脏表型。最后，感染诱导心脏和其他组织中两种溶菌酶基因的上调，用溶菌酶处理蚊子会以类似于感染表型的方式降低心率。这些数据展示了昆虫的免疫系统和循环系统之间整合的一个令人兴奋的新方面，即具有免疫活性的血细胞产生的因子，即一氧化氮，调节心脏生理学。
