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This chapter discusses the evolution of immune function. It emphasizes two points. First, the immune system is complex, with many responses that may act together or inhibit each other to determine the outcome of an infection. Using an immune response as an indicator of the host's resistance (or, more generally, its quality) is therefore problematic, as increased investment in a given immune response may well indicate increased susceptibility to a parasite. Second, resistance is a product of the interaction between a host and a parasite. Thus, we cannot understand the evolution of immune function without considering the co-evolution of the host's and the parasite's contributions to resistance. Indeed, as found in a more general context, mathematical models of the evolution of the host that do not consider the co-evolutionary response by the parasite can be misleading as their predictions can differ qualitatively from the co-evolutionary dynamics and equilibrium.

This chapter approaches the question of immune specificity from an evolutionary ecology perspective. For the sake of clarity, immune specificity is addressed on two levels. First, immune specificity is considered in the light of evidence for specific interactions between hosts and parasites. The importance of these specific interactions for questions concerning genetic diversity is then discussed. The second level on which immune specificity is addressed in the context of immune priming. It must be stressed that these two phenomena are almost certainly not mutually exclusive. For instance, the level of primed defences may be constrained by the innate defence capacity of an individual. Consequently, immune priming may play a role in the formation of specific interactions between hosts and parasites when re-infections are persistent or infections are chronic. Prior to concluding, the chapter considers sociality, and in particular immune defence within social insects.

This chapter discusses how and why short-term changes in physiological state (i.e., the acute stress response) alter immune responsiveness in insects. It also explores the ramifications of these effects for ecological immunologists.

Understanding how insect immunity is regulated requires studying the interactions of all those aspects of physiology that impact immunity. This includes both resistance and tolerance aspects of defence as well as all of the other assorted physiological systems of the insect that alter the immune response. It is hypothesized that an insect's innate immune responses is in the centre of a physiological net and the immune response is sensitive to changes throughout this net. This chapter tries to tie all of these physiological strands together and demonstrate how innate immunity alters the gross physiology of an insect and how the gross physiology, in turn, alters the immune response. An emergent property that falls out of this analysis is the prediction of several types of physiological collapse — these collapses result from positive-feedback loops that lead to amplified and damage-inducing immune/physiological responses.

This chapter begins by focusing on the parasites and pathogens known to attack or infect D. melanogaster (or other Drosophila species), from macro-parasites, such as parasitoids and mites to microbial (fungal and bacterial) pathogens to viruses. It concentrates on the main selection pressures for and against resistance against these parasites and pathogens. High resistance is selected for when the benefits it incurs outweigh its costs. For each parasite/pathogen, the chapter summarizes the existing knowledge on abundance in the field, fitness effects of parasitism/infection, and costs of resistance, where it distinguishes between costs of actual resistance and costs of the resistance mechanism. The second section of the chapter shifts the focus to the genomic level. Over the last few years several papers have been published where microarrays have been used to investigate D. melanogaster resistance to parasites and pathogens. The chapter considers what these studies are telling us about Drosophila resistance mechanisms and about the associated costs.

The placebo effect in the immune and endocrine system is basically a conditioned response, whereby classical conditioning plays a key role. Conditioned immunosuppression affects a number of immune mediators, like interleukin-2 and interferon-gamma. Some negative allergic reactions may be induced by the administration of nocebos. The responses of some hormones, like insulin, growth hormone, and cortisol, have been successfully conditioned. In addition, the hypothalamus-pituitary-adrenal axis may represent an important system in placebo and nocebo responsiveness.

This chapter examines the evolutionary genetics of immune defence, interpreting molecular evolutionary patterns in light of protein function to draw insight into how the immune response adapts to pathogen pressures. Topics discussed include evolutionary patterns in the antimicrobial immune response and the evolutionary patterns in the antiviral immune response.

This chapter discusses recent advances in our understanding of plasma proteins in the immune responses of the tobacco hornworm, Manduca sexta. It focuses on microbial pattern recognition proteins, and the complex interplay between proteinases, inactive homologues of proteinases, and proteinase inhibitors, all of which collaborate to regulate the proteolytic conversion of prophenoloxidase (proPO) to its active form, phenoloxidase (PO). It is becoming clearer that the proPO system is among the most rapidly deployed immune defences in insects. Its value to the host is shown by the fact that pathogens and parasites are frequently distinguished by the presence of anti-PO counter-adaptations. It is also especially interesting that vertebrate animals do not have a homologue of this system. The reason for this remains unknown.

The insect innate immune system is encoded by three major functional categories of genes that are involved in (1) recognition of invading microbes; (2) immune-signal amplification and transduction; and (3) effector mechanisms that mediate the killing and clearance of infectious micro-organisms. Despite its lack of adaptive immune mechanisms and antibody-mediated defences similar to those found in vertebrates, the innate immune system in insects is quite specific in its antimicrobial action. Once invading microbes are recognized through specific interaction between pattern-recognition receptors (PRRs) and pathogen-associated molecular patterns (PAMPs), a variety of defence reactions can be activated. This chapter discusses the specificity of the innate immune responses at the level of PRRs, with a major focus on the mosquito Anopheles gambiae as a model system. It first provides a general overview of the insects' PRR repertoire and highlights some of its most interesting features with regard to antimicrobial defence. It then provides detailed molecular and functional descriptions of some of the best characterized PRR families.

Multiple sclerosis (MS) is considered an autoimmune chronic inflammatory disease of the central nervous system (CNS) characterized by demyelination and axonal damage. The view of MS as a “two-stage disease”, with a predominant inflammatory demyelination in the early phase (relapsing-remitting MS form) and a subsequent secondary neurodegeneration in the early phase (secondary or primary progressive MS) of the disease, is now challenged by the demonstration that axonal destruction may occur independently of inflammation and may also produce it. Therefore, as CNS inflammation and degeneration can coexist throughout the course of the disease, MS may be a “simultaneous two-component disease”, in which the combination of neuroinflammation and neurodegeneration promotes irreversible disability. This chapter discusses factors that contribute to the pathogenesis of MS, immune surveillance in the CNS, regulation of immune responses in the inflamed CNS, initiation of T helper 1 (Th1)-mediated immune reactions in the inflamed CNS, amplification of Th1-mediated immune responses in inflamed CNS and tissue damage, and development of autoimmunity in MS.

This chapter compares the Drosophila group with mosquitoes and honeybees to disentangle common themes from specific components of immunity. Honeybees, for example, have a relatively small set of immune genes which demonstrate a high degree of conservatism. They are most intriguing when compared with non-social insects, as the differences between them are attributable to the evolution of sociality in bees and other Hymenoptera. The chapter highlights how the use of comparative genomics led to the unravelling of evolutionary novelties. Genes containing leucine-rich repeats are an example, which led to the discovery of a new complement-like mechanism in mosquitoes.

There is good physiological documentation of the survival of parasites (generally the ‘off-host’ stages) in environments that would be considered hostile to life and characterized by freezing, extreme desiccation, and so on. Equivalent adaptations may occur in free-living organisms, and are not therefore a feature of parasitism. However, these mechanisms are relevant to the ability of some parasites to persist in ecosystems at the margins of survival of life (as in hot and cold deserts). It is a feature of many such severe environments that constraints are relaxed periodically, even if very briefly, creating a ‘window of opportunity’ when transfer from host to host may occur. It is of even greater interest that, in some cases, transmission may continue even when external conditions appear to be most extreme and when it might be predicted that transmission should be arrested. In these situations, the host is typically regarded as the ‘safe’ environment while the external environment is viewed as hostile. In contrast, there is now abundant evidence that the host actually represents the most hostile environment in the parasite’s life cycle, constituting a finely tuned ‘killing machine’. The mechanisms of the various lethal factors are well documented, together with the reciprocal parasite adaptations for evasion and suppression of attack. This review takes an ecological perspective. Variations in parasite infectivity for particular host types and in host susceptibility to infection determine that some ‘environments’ (hosts) are more hostile than others. The shifting balance between prevailing host and parasite types determines the ability of parasites to persist in the spectrum of environments within the ecosystem. Even the ‘favourable’ environments (in which surviving infections reproduce) may be responsible for major mortality within parasite populations and this contributes to the regulation of the interactions.

This chapter examines the host's response to parasitism by considering behavioural and immunological defences to infectious disease. It focuses on the individual level by considering how primate immune systems defend against parasite infections, how animals use medicinal plants, and the avoidance of sick individuals. It also investigates the links between sexual selection and parasitism in primates, focusing in particular on mate choice.

This chapter begins with a brief review of the diversity of insect–symbiont interactions. It then proposes that symbionts are similar to constitutive defences: the insect always pays a metabolic cost. However, secondary symbionts can be lost easily if the selection pressure exerted by a parasitoid relaxes, for example. Aside from protection, there is another twist to the story. In most cases, these symbionts will be expressing pathogen-associated molecular patterns (PAMPs) similar to, or the same as, those of the pathogen. Moreover, the host needs to ensure that the symbionts cooperate. This establishes a very interesting perspective on the evolution of the insect's immune system: maintaining and managing symbionts could constitute a formidable selection pressure for the evolution of a policing system, such as immunity.

This chapter reviews the progress made in the past few years on antiviral defence mechanisms in Drosophila melanogaster, and discusses the relevance of these findings for our understanding of the complex interaction of viruses with their invertebrate or mammalian hosts. Topics covered include models of Drosophila virus infection, Drosophila immune response against viruses, antiviral defences in other insect or invertebrate species, and comparison with mammalian antiviral defences.

This chapter talks about certain observations and conclusions arrived at through the study of ecological immunology. The rate of parasitism and the level of immune response, for example, are often varied among individuals and populations. This variation, however, can be explained by ecological or demographic factors. The chapter also looks at the various costs that immune defences incur, including the cost of evolving and maintaining a defence, and the cost of using defence. It looks at the limiting resources for immune defences – energy, food, and nutrients – and how the capacity to immune-defend affects host fitness, where organisms face the problem of how to allocate their limited resources to defend, versus other demands, in order to achieve a maximum possible fitness. Finally, the chapter looks at the various elements of defence, namely resistance and tolerance. Resistance is where hosts reduce parasite numbers, while tolerance is where the damage caused by the infection is limited.

One of the most predictable episodes of a female insect's life is the timing of mate-encounter and mating. This chapter proposes that females are often subjected to predictable wounding during mating and that this wounding provides opportunity for environmental microbes to enter the female's haemocoel, thereby presenting immunological costs. It argues that this combination of factors is likely to lead to reproduction being a period of heightened immunological activity that has resulted in specific immune defence mechanisms and management systems that function to minimize costs while maximizing immunological efficacy. If true, these phenomena may provide valuable insights into how organisms with mechanistically simple immune systems protect themselves against a complex pathogenic world, and may also provide logistic opportunities to better study immunity in the wild.

By reducing immune function, trace metal deficiencies may substantially contribute to the global burden of diarrhea, pneumonia, and malaria. Human activities may be contributing to trace metal deficiency in soils and plants by exacerbating the preponderance of cereals and cash crops that reduce food diversity and micronutrient intake. Adaptive strategies are needed to reverse these trends. Anthropogenic activities have led to increased toxic metal exposure, and effects on human hosts need clarification. Metal toxicities can also impair the immune system and hence increase the susceptibility to infectious pathogens. Climate change affects metal speciation and the build-up of trace elements in the human food chain, with as yet unknown outcomes on infectious disease. Food processing and the use of metallic nanomaterials can alter human exposure to metals in ways that can influence the host–pathogen competition for metals. The effects of metals on human health may also be mediated through modification of the epigenome, conferring drug resistance on pathogenic bacteria and enhancing/ reducing human tolerance to infectious parasites. The emerging metals cerium, gadolinium, lanthanum, and yttrium constitute another driver of change in metal exposure and may potentially modulate the immune system with unknown consequences for human health.

Several metals play important roles in host cell and microbial metabolism because they form a part of central enzymes that are essential, for example, for DNA synthesis, cellular respiration, and key metabolic pathways. The availability of these metals differentially impact on host antimicrobial immune responses as well as on microbial defenses against them (Botella et al. 2012). Thus, during infection, host cells attempt to gain sufficient access to these metals or to limit the availability of these factors for microbes; this is thought to play a decisive role in the course of infections. Accordingly, subtle changes in the metabolism of these metals and their distribution throughout the body occur: microbes activate different pathways to secure a sufficient supply of these metals needed for their pathogenicity and proliferation as well as to mount effective defenses against the host immune system. This review focuses on the role of iron in the host–pathogen interplay. A brief discussion is included on the role of zinc, manganese, and copper for host–pathogen interaction, immune function, and their alteration by the inflammatory response.

This chapter explains the biological synergies of malnutrition, parasitic and infectious diseases, and immune response that are specific to HIV transmission, and widespread among poor populations in Africa, Asia, Latin America, and the transition countries. It draws on extensive medical literature that demonstrates that malnutrition, malaria, soil-transmitted helminths and other worms, schistosomiasis (and its genital lesions and inflammation, which resemble sexually transmitted diseases, or STDs), and other parasites increase HIV viral load and viral shedding, and hence increase the risk of HIV transmission.