Kissing bugs have long served as models to study many aspects of insect physiology. They also serve as vectors for the parasite Trypanosoma cruzi that causes Chagas disease in humans. The overall success of insects is due, in part, to their ability to recognize parasites and pathogens as non-self and to eliminate them using their innate immune system. This immune system comprises physical barriers, cellular responses (phagocytosis, nodulation and encapsulation), and humoral factors (antimicrobial peptides and the prophenoloxidase cascade). Trypanosoma cruzi survives solely in the gastrointestinal (GI) tract of the vector; if it migrates to the hemocoel it is eliminated. Kissing bugs may not mount a vigorous immune response in the GI tract to avoid eliminating obligate symbiotic microbes on which they rely for survival. Here we describe the current knowledge of innate immunity in kissing bugs and new opportunities using genomic and transcriptomic approaches to study the complex triatomine-trypanosome-microbiome interactions.
Keywords: AMPs; Innate immunity; Kissing bug; Microbiome; Rhodnius prolixus; Triatomine; Trypanosoma cruzi; Trypanosoma rangeli.
Copyright © 2019. Published by Elsevier Ltd.