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Wounding occurs across multicellular organisms. Wounds can affect host mobility and reproduction, with ecological consequences for competitive interactions and predator-prey dynamics. Wounds are also entry points for pathogens. An immune response is activated upon injury, resulting in the deposition of the brown-black pigment melanin in insects. Despite the abundance of immunity studies in the laboratory and the potential ecological and evolutionary implications of wounding, the prevalence of wounding in wild-collected insects is rarely systematically explored. We investigated the prevalence and potential causes of wounds in wild-collected Drosophilidae flies. We found that 31% of Drosophila melanogaster were wounded or damaged. The abdomen was the most frequently wounded body part, and females were more likely to have melanized patches on the ventral abdomen, compared with males. Encapsulated parasitoid egg frequency was approximately 10%, and just under 1% of Drosophilidae species had attached mites, which also caused wounds. Wounding is prevalent in D. melanogaster, likely exerting selection pressure on host immunity for two reasons: on a rapid and efficient wound repair and on responding efficiently to opportunistic infections. Wounding is thus expected to be an important driver of immune system evolution and to affect individual fitness and population dynamics.
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A fundamental goal in infection biology is to understand the emergence of variation in pathogen virulence-here defined as the decrease in host fitness caused by a pathogen. To uncover the sources of such variation, virulence can be decomposed into both host- and pathogen-associated components. However, decomposing virulence can be challenging owing to complex within-host pathogen dynamics such as bifurcating infections, which recently received increased empirical and theoretical attention. Bifurcating infections are characterized by the emergence of two distinct infection types: (i) terminal infections with high pathogen loads resulting in rapid host death, and (ii) persistent infections with lower loads and delayed host death. Here, we propose to use discrete mixture models to perform separate virulence decompositions for each infection type. Using this approach, we reanalysed a recently published experimental dataset on bacterial load and survival in Drosophila melanogaster. This analysis revealed several advantages of the new approach, most importantly the generation of a more comprehensive picture of the varying sources of virulence in different bacterial species. Beyond this application, our approach could provide valuable information for ground-truthing and improving theoretical models of within-host infection dynamics, which are developed to predict variation in infection outcome and pathogen virulence.
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Drosophila melanogaster , Animais , Virulência , Carga BacterianaRESUMO
Following an infection, hosts cannot always clear the pathogen, instead either dying or surviving with a persistent infection. Such variation is ecologically and evolutionarily important because it can affect infection prevalence and transmission, and virulence evolution. However, the factors causing variation in infection outcomes, and the relationship between clearance and virulence are not well understood. Here we show that sustained persistent infection and clearance are both possible outcomes across bacterial species showing a range of virulence in Drosophila melanogaster. Variation in virulence arises because of differences in the two components of virulence: bacterial infection intensity inside the host (exploitation), and the amount of damage caused per bacterium (per parasite pathogenicity). As early-phase exploitation increased, clearance rates later in the infection decreased, whereas there was no apparent effect of per parasite pathogenicity on clearance rates. Variation in infection outcomes is thereby determined by how virulence - and its components - relate to the rate of pathogen clearance. Taken together we demonstrate that the virulence decomposition framework is broadly applicable and can provide valuable insights into host-pathogen interactions.
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Evolução Biológica , Parasitos , Animais , Bactérias , Drosophila melanogaster , Infecção Persistente , VirulênciaRESUMO
Abstract: Sexual dimorphism in somatic investment may be shaped by two distinct forms of sexual conflict; under intralocus sexual conflict (IASC), males and females have different optimal levels of somatic investment but are constrained from reaching their respective optima by their shared genome, while under interlocus sexual conflict (IRSC), males and females have different optimal sexual strategies, which could have direct or indirect effects on levels of somatic investment. We investigated effects of IASC and IRSC on two aspects of somatic investment, immune defence strategies and longevity, using previously established female-limited experimental evolution lines in Drosophila melanogaster. We found little evidence for any effect of either type of sexual conflict on investment in the immune defence resistance or tolerance. Nor did we find convincing evidence that longevity is subject to IASC in this species. However, we did find evidence that increased female control over mating rate had important and opposite effects on longevity between the sexes. Specifically, females that had adapted to high levels of female control over mating had a longer lifespan when kept in mixed-sex groups, while males had shorter longevity, perhaps due to increased investment in post-copulatory sexual selection. These novel results show that female control over mating rates may have important and unexpected effects on patterns of somatic investment. Significance statement: Sexual conflict occurs between the two sexes over numerous life history traits, and it is complex to disentangle how these traits interact and affect each other. Here we use a long-term evolution experiment to investigate sexual dimorphism in somatic maintenance. We found no effect of feminising the X chromosome on female immune defence. However, we did find that increased female control over mating rate resulted in longer female lifespan, but reduced male lifespan, and that these effects were dependent on social context (isolated or in mixed-sex groups). Unlike previous studies on the effect of sexual conflict on longevity, our experiment did not manipulate environmental conditions nor the adult sex ratio, which is likely to reduce both pre- and post-copulatory sexual selection. Supplementary Information: The online version contains supplementary material available at 10.1007/s00265-022-03231-4.
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Immune priming describes the phenomenon whereby after a primary pathogen exposure, a host more effectively fights a lethal secondary exposure (challenge) to the same pathogen. Conflicting evidence exists for immune priming in invertebrates, potentially due to heterogeneity across studies in the pathogen species tested, the antigen preparation for the primary exposure, and the phenotypic trait used to test for priming. To explore these factors, we injected Drosophila melanogaster with one of two bacterial species, Lactococcus lactis or Providencia burhodogranariea, which had either been heat-killed or inactivated with formaldehyde, or we injected a 1:1 mixture of the two inactivation methods. Survival and resistance (the inverse of bacterial load) were assessed after a live bacterial challenge. In contrast to our predictions, none of the primary exposure treatments provided a survival benefit after challenge compared to the controls. Resistance in the acute phase, i.e., 1 day post-challenge, separated into a lower- and higher-load group, however, neither group varied according to the primary exposure. In the chronic phase, i.e., 7 days post-challenge, resistance did not separate into two groups, and it was also unaffected by the primary exposure. Our multi-angled study supports the view that immune priming may require specific circumstances to occur, rather than it being a ubiquitous aspect of insect immunity.
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Mating causes considerable alterations in female physiology and behaviour, and immune gene expression, partly due to proteins transferred from males to females during copulation. The magnitude of these phenotypic changes could be driven by the genotypes of males and females, as well as their interaction. To test this, we carried out a series of genotype-by-genotype (G × G) experiments using Drosophila melanogaster populations from two distant geographical locations. We expected lines to have diverged in male reproductive traits and females to differ in their responses to these traits. We examined female physiological and behavioural post-mating responses to male mating traits, that is behaviour and ejaculate composition, in the short to mid-term (48 hr) following mating. We then explored whether a sexually transferred molecule, sex peptide (SP), is the mechanism behind our observed female post-mating responses. Our results show that the genotypes of both sexes as well as the interaction between male and female genotypes affect mating and post-mating reproductive traits. Immune gene expression of three candidate genes increased in response to mating and was genotype-dependent but did not show a G × G signature. Males showed genotype-dependent SP expression in the 7 days following eclosion, but female genotypes showed no differential sensitivity to the receipt of SP. The two genotypes demonstrated clear divergence in physiological traits in short- to mid-term responses to mating, but the longer-term consequences of these initial dynamics remain to be uncovered.
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Evolução Biológica , Proteínas de Drosophila/fisiologia , Drosophila melanogaster/genética , Peptídeos/fisiologia , Reprodução/genética , Comportamento Sexual Animal , Animais , Feminino , Masculino , Reprodução/imunologiaRESUMO
Social environments have been shown to have multiple effects on individual immune responses. For example, increased social contact might signal greater infection risk and prompt a prophylactic upregulation of immunity. This differential investment of resources may in part explain why social environments affect ageing and lifespan. Our previous work using Drosophila melanogaster showed that single-sex social contact reduced lifespan for both sexes. Here, we assess how social interactions (isolation or contact) affect susceptibility to infection, phagocytotic activity and expression of a subset of immune- and stress-related genes in young and old flies of both sexes. Social contact had a neutral, or even improved, effect on post-infection lifespan in older flies and reduced the expression of stress response genes in females; however, it reduced phagocytotic activity. Overall, the effects of social environment were complex and largely subtle and do not indicate a consistent effect. Together, these findings indicate that social contact in D. melanogaster does not have a predictable impact on immune responses and does not simply trade-off immune investment with lifespan.
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Envelhecimento/fisiologia , Drosophila melanogaster/microbiologia , Comportamento Social , Animais , Bactérias/imunologia , Fenômenos Fisiológicos Bacterianos , Drosophila melanogaster/imunologia , Drosophila melanogaster/fisiologia , Feminino , Interações Hospedeiro-Patógeno/fisiologia , Masculino , Fatores SexuaisRESUMO
Hosts can alter their strategy towards pathogens during their lifetime; that is, they can show phenotypic plasticity in immunity or life history. Immune priming is one such example, where a previous encounter with a pathogen confers enhanced protection upon secondary challenge, resulting in reduced pathogen load (i.e., resistance) and improved host survival. However, an initial encounter might also enhance tolerance, particularly to less virulent opportunistic pathogens that establish persistent infections. In this scenario, individuals are better able to reduce the negative fecundity consequences that result from a high pathogen burden. Finally, previous exposure may also lead to life-history adjustments, such as terminal investment into reproduction. Using different Drosophila melanogaster host genotypes and two bacterial pathogens, Lactococcus lactis and Pseudomonas entomophila, we tested whether previous exposure results in resistance or tolerance and whether it modifies immune gene expression during an acute-phase infection (one day post-challenge). We then asked whether previous pathogen exposure affects chronic-phase pathogen persistence and longer-term survival (28 days post-challenge). We predicted that previous exposure would increase host resistance to an early stage bacterial infection while it might come at a cost to host fecundity tolerance. We reasoned that resistance would be due in part to stronger immune gene expression after challenge. We expected that previous exposure would improve long-term survival, that it would reduce infection persistence, and we expected to find genetic variation in these responses. We found that previous exposure to P. entomophila weakened host resistance to a second infection independent of genotype and had no effect on immune gene expression. Fecundity tolerance showed genotypic variation but was not influenced by previous exposure. However, L. lactis persisted as a chronic infection, whereas survivors cleared the more pathogenic P. entomophila infection. To our knowledge, this is the first study that addresses host tolerance to bacteria in relation to previous exposure, taking a multi-faceted approach to address the topic. Our results suggest that previous exposure comes with transient costs to resistance during the early stage of infection in this host-pathogen system and that infection persistence may be bacterium-specific.
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Drosophila melanogaster , Interações Hospedeiro-Patógeno , Animais , Bactérias , Fertilidade , GenótipoRESUMO
The transfer of immunity from mother to offspring is a central way to endow the offspring with increased protection against pathogens. This phenomenon is not only found within the vertebrate domain: in some circumstances, invertebrate mothers can also give their offspring an immune kick-start, which is termed trans-generational immune priming (TGIP). TGIP has been uncovered for a number of invertebrate species, but it is not ubiquitously evident. The reasons for which are not known. In this issue of Molecular Ecology, Tate, Andolfatto, Demuth, and Graham () probe the molecular underpinnings of TGIP in concert with the temporal dynamics of the response in the red flour beetle, Tribolium castaneum, infected with the bacterium Bacillus thuringiensis (Figure ). They provide previously lacking evidence for the repeatability of TGIP, meaning that when averaged across several experiments, the offspring of mothers infected with heat-killed bacteria had better survival when they themselves were infected with live bacteria than offspring from mothers that had not encountered the bacterium. In a detailed temporal examination of the offspring's acute infection phase (zero to 24 hr after infection), Tate et al. () follow T. castaneum's gene regulation responses to infection while simultaneously documenting bacterial load. Such an approach gives considerable insight into the physiological processes that occur in primed offspring, and a first glance at a potential role for tolerance and effects on host metabolism that might even resemble trained immunity, which is a form of innate immune memory in vertebrates.
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Bacillus thuringiensis , Besouros , Tribolium , Animais , Regulação da Expressão GênicaRESUMO
The Down syndrome cell adhesion molecule 1 (Dscam1) gene is an extraordinary example of diversity: by combining alternatively spliced exons, thousands of isoforms can be produced from just one gene. So far, such diversity in this gene has only been found in insects and crustaceans, and its essential part in neural wiring has been well-characterized for Drosophila melanogaster. Ten years ago evidence from D. melanogaster showed that the Dscam1 gene is involved in insect immune defense and work on Anopheles gambiae indicated that it is a hypervariable immune receptor. These exciting findings showed that via processes of somatic diversification insects have the possibility to produce unexpected immune molecule diversity, and it was hypothesized that Dscam1 could provide the mechanistic underpinnings of specific immune responses. Since these first publications the quest to understand the function of this gene has uncovered fascinating insights from insects and crustaceans. However, we are still far from a complete understanding of how Dscam1 functions in relation to parasites and pathogens and its full relevance for the immune system. In this Hypothesis and Theory article, we first briefly introduce Dscam1 and what we know so far about how it might function in immunity. By focusing on seven questions, we then share our sometimes contrasting thoughts on what the evidence tells us so far, what essential experiments remain to be done, and the future prospects, with the aim to provide a multiangled view on what this fascinating gene has to do with immune defense.
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BACKGROUND: Increasing temperatures are predicted to strongly impact host-parasite interactions, but empirical tests are rare. Host species that are naturally exposed to a broad temperature spectrum offer the possibility to investigate the effects of elevated temperatures on hosts and parasites. Using three-spined sticklebacks, Gasterosteus aculeatus L., and tapeworms, Schistocephalus solidus (Müller, 1776), originating from a cold and a warm water site of a volcanic lake, we subjected sympatric and allopatric host-parasite combinations to cold and warm conditions in a fully crossed design. We predicted that warm temperatures would promote the development of the parasites, while the hosts might benefit from cooler temperatures. We further expected adaptations to the local temperature and mutual adaptations of local host-parasite pairs. RESULTS: Overall, S. solidus parasites grew faster at warm temperatures and stickleback hosts at cold temperatures. On a finer scale, we observed that parasites were able to exploit their hosts more efficiently at the parasite's temperature of origin. In contrast, host tolerance towards parasite infection was higher when sticklebacks were infected with parasites at the parasite's 'foreign' temperature. Cold-origin sticklebacks tended to grow faster and parasite infection induced a stronger immune response. CONCLUSIONS: Our results suggest that increasing environmental temperatures promote the parasite rather than the host and that host tolerance is dependent on the interaction between parasite infection and temperature. Sticklebacks might use tolerance mechanisms towards parasite infection in combination with their high plasticity towards temperature changes to cope with increasing parasite infection pressures and rising temperatures.
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Cestoides/fisiologia , Infecções por Cestoides/veterinária , Interações Hospedeiro-Parasita/fisiologia , Smegmamorpha/fisiologia , Smegmamorpha/parasitologia , Temperatura , Adaptação Biológica/imunologia , Adaptação Biológica/fisiologia , Animais , Cestoides/crescimento & desenvolvimento , Cestoides/imunologia , Cestoides/patogenicidade , Infecções por Cestoides/imunologia , Infecções por Cestoides/parasitologia , Temperatura Baixa , Resistência à Doença , Meio Ambiente , Doenças dos Peixes/imunologia , Doenças dos Peixes/parasitologia , Interações Hospedeiro-Parasita/imunologia , Temperatura Alta , Tolerância Imunológica , Rim , Leucócitos/imunologia , Parasitos/crescimento & desenvolvimento , Parasitos/patogenicidade , Parasitos/fisiologia , Smegmamorpha/crescimento & desenvolvimento , Smegmamorpha/imunologiaRESUMO
Central to the basis of ecological immunology are the ideas of costs and trade-offs between immunity and life history traits. As a physical barrier, the insect cuticle provides a key resistance trait, and Tenebrio molitor shows phenotypic variation in cuticular colour that correlates with resistance to the entomopathogenic fungus Metarhizium anisopliae. Here we first examined whether there is a relationship between cuticular colour variation and two aspects of cuticular architecture that we hypothesised may influence resistance to fungal invasion through the cuticle: its thickness and its porosity. Second, we tested the hypothesis that tyrosine, a semi-essential amino acid required for immune defence and cuticular melanisation and sclerotisation, can act as a limiting resource by supplementing the larval diet and subsequently examining adult cuticular colouration and thickness. We found that stock beetles and beetles artificially selected for extremes of cuticular colour had thicker less porous cuticles when they were darker, and thinner more porous cuticles when they were lighter, showing that colour co-varies with two architectural cuticular features. Experimental supplementation of the larval diet with tyrosine led to the development of darker adult cuticle and affected thickness in a sex-specific manner. However, it did not affect two immune traits. The results of this study provide a mechanism for maintenance of cuticular colour variation in this species of beetle; darker cuticles are thicker, but their production is potentially limited by resource constraints and differential investments in resistance mechanisms between the sexes.
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Fenótipo , Pigmentação , Seleção Genética , Tenebrio/fisiologia , Tirosina/administração & dosagem , Animais , Cor , Suplementos Nutricionais/análise , Feminino , Hemócitos/metabolismo , Larva/genética , Larva/crescimento & desenvolvimento , Larva/imunologia , Larva/fisiologia , Masculino , Monofenol Mono-Oxigenase/metabolismo , Pigmentação/efeitos dos fármacos , Tenebrio/genética , Tenebrio/crescimento & desenvolvimento , Tenebrio/imunologiaRESUMO
Tolerance, the ability of a host to limit the negative fitness effects of a given parasite load, is now recognised as an important host defence strategy in animals. Together with resistance, the ability of a host to limit parasite load, these two host strategies represent two disparate host responses to parasites, each with different predicted evolutionary consequences: resistance is predicted to reduce parasite prevalence, whereas tolerance could be neutral towards, or increase, parasite prevalence in a population. The distinction between these two strategies might have far-reaching epidemiological consequences. Classically, a reaction norm defines host tolerance because it depicts the change in host fitness as a function of parasite load, where a shallow negative slope indicates that host fitness slowly deteriorates as parasite load increases (i.e., high tolerance). Despite the fact that tolerance was only recently acknowledged to be an important component in an animal's immune repertoire, it is frequently referenced, so our aim is to emphasise the current advances on the topic. We begin by summarising the ways in which biologists measure the two components of tolerance, parasite load and fitness, as well as the ways in which the concept has been defined (i.e., point and range tolerance). It is common to test for variation in host tolerance according to intrinsic, innate factors, where variation exists among populations, genders or genotypes. Such variation in tolerance is pervasive across animal taxa, and we briefly review some of the mechanistic bases of variation that have recently begun to be explored. Three further novel advancements in the tolerance field are the appreciation of the role of extrinsic, environmental factors on tolerance, host tolerance in multi-host-parasite systems and individual-based approaches to tolerance measures. We explore these topics using recent examples and suggest some future perspectives. It is becoming increasingly clear that an appreciation of tolerance as a defence strategy can provide significant insights into how hosts coexist with parasites.
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Aptidão Genética/imunologia , Modelos Imunológicos , Doenças Parasitárias em Animais/imunologia , Animais , Variação Genética , Humanos , Doenças Parasitárias em Animais/genéticaRESUMO
Mounting and maintaining an effective immune response in the face of infection can be costly. The outcome of infection depends on two host immune strategies: resistance and tolerance. Resistance limits pathogen load, while tolerance reduces the fitness impact of an infection. While resistance strategies are well studied, tolerance has received less attention, but is now considered to play a vital role in host-pathogen interactions in animals. A major challenge in ecoimmunology is to understand how some hosts maintain their fitness when infected while others succumb to infection, as well as how extrinsic, environmental factors, such as diet, affect defense. We tested whether dietary restriction through yeast (protein) limitation affects resistance, tolerance, and fecundity in Drosophila melanogaster. We predicted that protein restriction would reveal costs of infection. Because infectious diseases are not always lethal, we tested resistance and tolerance using two bacteria with low lethality: Escherichia coli and Lactococcus lactis. We then assayed fecundity and characterized bacterial infection pathology in individual flies at two acute phase time points after infection. As expected, our four fecundity measures all showed a negative effect of a low-protein diet, but contrary to predictions, diet did not affect resistance to either bacteria species. We found evidence for diet-induced and time-dependent variation in host tolerance to E. coli, but not to L. lactis. Furthermore, the two bacteria species exhibited remarkably different infection profiles, and persisted within the flies for at least 7 days postinfection. Our results show that acute phase infections do not necessarily lead to fecundity costs despite high bacterial loads. The influence of intrinsic variables such as genotype are the prevailing factors that have been studied in relation to variation in host tolerance, but here we show that extrinsic factors should also be considered for their role in influencing tolerance strategies.
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Fungus-growing ants (Attini) have evolved an obligate dependency upon a basidiomycete fungus that they cultivate as their food. Less well known is that the crop fungus is also used by many attine species to cover their eggs, larvae and pupae. The adaptive functional significance of this brood covering is poorly understood. One hypothesis to account for this behaviour is that it is part of the pathogen protection portfolio when many thousands of sister workers live in close proximity and larvae and pupae are not protected by cells, as in bees and wasps, and are immobile. We performed behavioural observations on brood covering in the leaf-cutting ant Acromyrmex echinatior, and we experimentally manipulated mycelial cover on pupae and exposed them to the entomopathogenic fungus Metarhizium brunneum to test for a role in pathogen resistance. Our results show that active mycelial brood covering by workers is a behaviourally plastic trait that varies temporally, and across life stages and castes. The presence of a fungal cover on the pupae reduced the rate at which conidia appeared and the percentage of pupal surface that produced pathogen spores, compared to pupae that had fungal cover experimentally removed or naturally had no mycelial cover. Infected pupae with mycelium had higher survival rates than infected pupae without the cover, although this depended upon the time at which adult sister workers were allowed to interact with pupae. Finally, workers employed higher rates of metapleural gland grooming to infected pupae without mycelium than to infected pupae with mycelium. Our results imply that mycelial brood covering may play a significant role in suppressing the growth and subsequent spread of disease, thus adding a novel layer of protection to their defence portfolio.
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Formigas/microbiologia , Formigas/fisiologia , Basidiomycota/fisiologia , Metarhizium/fisiologia , Comportamento de Nidação , Simbiose , Animais , Formigas/crescimento & desenvolvimento , Pupa/crescimento & desenvolvimento , Pupa/microbiologia , Pupa/fisiologiaRESUMO
Down syndrome cell adhesion molecule 1 (Dscam1) has wide-reaching and vital neuronal functions although the role it plays in insect and crustacean immunity is less well understood. In this study, we combine different approaches to understand the roles that Dscam1 plays in fitness-related contexts in two model insect species. Contrary to our expectations, we found no short-term modulation of Dscam1 gene expression after haemocoelic or oral bacterial exposure in Tribolium castaneum, or after haemocoelic bacterial exposure in Drosophila melanogaster. Furthermore, RNAi-mediated Dscam1 knockdown and subsequent bacterial exposure did not reduce T. castaneum survival. However, Dscam1 knockdown in larvae resulted in adult locomotion defects, as well as dramatically reduced fecundity in males and females. We suggest that Dscam1 does not always play a straightforward role in immunity, but strongly influences behaviour and fecundity. This study takes a step towards understanding more about the role of this intriguing gene from different phenotypic perspectives.
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The relationship between robustness and evolvability is a long-standing question in evolution. Heat shock protein 90 (HSP90), a molecular chaperone, has been identified as a potential capacitor for evolution, since it allows for the accumulation and release of cryptic genetic variation, and also for the regulation of novel genetic variation through transposon activity. However, to date, it is unknown whether Hsp90 expression is regulated upon demand (i.e. when the release of cryptic genetic variation is most needed). Here, we show that Hsp90 has reduced transcription under conditions where the mobilization of genetic variation could be advantageous. We designed a situation that indicates a stressful environment but avoids the direct effects of stress, by placing untreated (focal) red flour beetles, Tribolium castaneum, into groups together with wounded conspecifics, and found a consistent reduction in expression of two Hsp90 genes (Hsp83 and Hsp90) in focal beetles. We moreover observed a social transfer of immunity in this non-eusocial insect: there was increased activity of the phenoloxidase enzyme and downregulation of the immune regulator, imd. Our study poses the exciting question of whether evolvability might be regulated through the use of information derived from the social environment.
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Regulação para Baixo , Proteínas de Choque Térmico HSP90/genética , Proteínas de Insetos/genética , Tribolium/fisiologia , Animais , Sinais (Psicologia) , Feminino , Proteínas de Choque Térmico HSP90/metabolismo , Proteínas de Insetos/metabolismo , Masculino , Monofenol Mono-Oxigenase/genética , Monofenol Mono-Oxigenase/metabolismo , Comportamento Social , Tribolium/enzimologia , Tribolium/genéticaRESUMO
Animals are inhabited by a diverse community of microorganisms. The relevance of such microbiota is increasingly being recognized across a broad spectrum of species, ranging from sponges to primates, revealing various beneficial roles that microbes can play. The red flour beetle Tribolium castaneum represents a well-established experimental model organism for studying questions in ecology and evolution, however, the relevance of its microbial community is still largely unknown. T. castaneum larvae orally exposed to bacterial components of the entomopathogen Bacillus thuringiensis bv. tenebrionis showed increased survival upon a subsequent challenge with spores of this bacterium. To investigate whether T. castaneum microbiota plays a role in this phenomenon, we established a protocol for raising microbe-free larvae and subsequently tested whether they differ in their ability to mount such a priming response. Here we demonstrate that larvae with significantly lowered microbial loads, show decreased survival upon secondary challenge with B. thuringiensis bv. tenebrionis spores, compared to animals that were allowed to regain their microbiota before priming. Although the exact mechanism of oral immune priming is unclear, we here suggest that microbiota plays a crucial role in oral immune priming in this species.
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Evidence is accumulating for a memory-like phenomenon in the immune defence of invertebrates. Down syndrome cell adhesion molecule (Dscam) has been proposed as a key candidate for a somatically diversified receptor system in the crustaceans and insects (Pancrustacea) that could enable challenge-specific protection. However, what is the evidence for an involvement of Dscam in pancrustacean immune memory, and in particular specificity? Here we review the current state of the art, and discuss hypotheses of how Dscam could be involved in immunity. We conclude that while there is increasing evidence for the involvement of Dscam in pancrustacean immunity, crucial experiments to address whether it plays a role in specificity upon secondary encounter with a pathogen still remain to be done.