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Whether specific immune protection after initial pathogen exposure (immune memory) occurs in invertebrates has long been uncertain. The absence of antibodies, B-cells and T-cells, and the short lifespans of invertebrates led to the hypothesis that immune memory does not occur in these organisms. However, research in the past two decades has supported the existence of immune memory in several invertebrate groups, including Ctenophora, Cnidaria, Nematoda, Mollusca and Arthropoda. Interestingly, some studies have demonstrated immune memory that is specific to the parasite strain. Nonetheless, other work does not provide support for immune memory in invertebrates or offers only partial support. Moreover, the expected biphasic immune response, a characteristic of adaptive immune memory in vertebrates, varies within and between invertebrate species. This variation may be attributed to the influence of biotic or abiotic factors, particularly parasites, on the outcome of immune memory. Despite its critical importance for survival, the role of phenotypic plasticity in immune memory has not been systematically examined in the past two decades. Additionally, the features of immune responses occurring in diverse environments have yet to be fully characterized.
Whether specific immune protection after initial pathogen exposure (immune memory) occurs in invertebrates has long been uncertain. The absence of antibodies, B-cells and T-cells, and the short lifespans of invertebrates led to the hypothesis that immune memory does not occur in these organisms. However, research in the past two decades has supported the existence of immune memory in several invertebrate groups, including Ctenophora, Cnidaria, Nematoda, Mollusca and Arthropoda. Interestingly, some studies have demonstrated immune memory that is specific to the parasite strain. Nonetheless, other work does not provide support for immune memory in invertebrates or offers only partial support. Moreover, the expected biphasic immune response, a characteristic of adaptive immune memory in vertebrates, varies within and between invertebrate species. This variation may be attributed to the influence of biotic or abiotic factors, particularly parasites, on the outcome of immune memory. Despite its critical importance for survival, the role of phenotypic plasticity in immune memory has not been systematically examined in the past two decades. Additionally, the features of immune responses occurring in diverse environments have yet to be fully characterized.
The assumption that the invertebrate immune system lacks memory and specificity has changed over time: many studies now indicate that a primary exposure of the host to a pathogen increases its resistance to a subsequent lethal challenge, a phenomenon known as immune priming. One group of insects in which immune priming has been little investigated is the hematophagous triatomine bugs. Herein, we tested the capability of the kissing bug Rhodnius pallescens Barber (Hemiptera: Reduviidae; hereafter kissing bugs), the vector of Chagas disease, to resist entomopathogenic fungi. Laboratory kissing bugs free of Wolbachia and Trypanosoma spp. as well as kissing bugs collected from the wild were used for tests with the entomopathogen Beauveria bassiana (Balsamo) Vuillemin (Hypocreales: Cordycipitaceae). Against laboratory kissing bugs, the fungus remained virulent for 94 d, indicating long-term viability. Kissing bugs collected from the wild that were exposed to a nonlethal dose of the fungus did not show increased survival against a lethal dose compared with controls inoculated with the lethal dose. However, kissing bugs inoculated with a nonlethal dose had higher levels of total phenoloxidase than control kissing bugs. Although the fungus activates the immune system of the kissing bugs, other variables may influence survival in the face of infection. Moreover, the lethality of the same strain was lower against wild kissing bugs, suggesting that the presence of symbionts or parasites influence the fungus–triatome (host) interaction. This work is one of the few studies that have investigated the fungus–host interaction in terms of immune priming in a hematophagous insect of public health importance. Implications are discussed.
This review summarizes the interactions between Trypanosoma cruzi, the etiologic agent of Chagas disease, its vectors, triatomines, and the diverse intestinal microbiota of triatomines, which includes mutualistic symbionts, and highlights open questions. T. cruzi strains show great biological heterogeneity in their development and their interactions. Triatomines differ from other important vectors of diseases in their ontogeny and the enzymes used to digest blood. Many different bacteria colonize the intestinal tract of triatomines, but only Actinomycetales have been identified as mutualistic symbionts. Effects of the vector on T. cruzi are indicated by differences in the ability of T. cruzi to establish in the triatomines and in colonization peculiarities, i.e., proliferation mainly in the posterior midgut and rectum and preferential transformation into infectious metacyclic trypomastigotes in the rectum. In addition, certain forms of T. cruzi develop after feeding and during starvation of triatomines. Negative effects of T. cruzi on the triatomine vectors appear to be particularly evident when the triatomines are stressed and depend on the T. cruzi strain. Effects on the intestinal immunity of the triatomines are induced by ingested blood-stage trypomastigotes of T. cruzi and affect the populations of many non-symbiotic intestinal bacteria, but not all and not the mutualistic symbionts. After the knockdown of antimicrobial peptides, the number of non-symbiotic bacteria increases and the number of T. cruzi decreases. Presumably, in long-term infections, intestinal immunity is suppressed, which supports the growth of specific bacteria, depending on the strain of T. cruzi. These interactions may provide an approach to disrupt T. cruzi transmission.
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