Inflammation and oxidative stress in vertebrate host-parasite systems.
ABSTRACT Innate, inflammation-based immunity is the first line of vertebrate defence against micro-organisms. Inflammation relies on a number of cellular and molecular effectors that can strike invading pathogens very shortly after the encounter between inflammatory cells and the intruder, but in a non-specific way. Owing to this non-specific response, inflammation can generate substantial costs for the host if the inflammatory response, and the associated oxygen-based damage, get out of control. This imposes strong selection pressure that acts to optimize two key features of the inflammatory response: the timing of activation and resolution (the process of downregulation of the response). In this paper, we review the benefits and costs of inflammation-driven immunity. Our aim is to emphasize the importance of resolution of inflammation as a way of maintaining homeostasis against oxidative stress and to prevent the 'horror autotoxicus' of chronic inflammation. Nevertheless, host immune regulation also opens the way to pathogens to subvert host defences. Therefore, quantifying inflammatory costs requires assessing (i) short-term negative effects, (ii) delayed inflammation-driven diseases, and (iii) parasitic strategies to subvert inflammation.
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ABSTRACT: Parasites influence allocation trade-offs between reproduction and self-maintenance and consequently shape host life-history traits. The host microbiome includes pathogenic and commensal micro-organisms that are remarkable in their diversity and ubiquity. However, experimental studies investigating whether the microbiome shapes host reproduction are still lacking.In this study, we tested whether the microbiome affects three important components of bird reproduction, namely (i) the maternal transfer of anti-microbial compounds to the eggs, (ii) the development of nestlings and (iii) the trade-off between reproduction and self-maintenance, here measured by the oxidative costs of reproduction.We experimentally modified the microbiome of wild breeding Great tits (Parus major) by spraying nests with liquid solution that either favoured or inhibited bacterial growth compared to a control. These treatments modified the bacterial communities in the nests and on adult feathers.We found that females from the treatment that decreased bacterial densities in the nests laid eggs with less carotenoids than females from the control, while we found no significant effect of increasing bacterial densities and modifying community composition compared to the control. Nestlings exposed to decreased bacterial densities grew faster and had longer tarsus length at fledging. Moreover, our analyses revealed that the relationship between investment in reproduction and oxidative damage was affected by the treatments. Adults raising larger clutches suffered higher oxidative damage in control nests, whereas this oxidative cost of reproduction was not detected when we modified bird microbiome.Our study provides experimental evidence for an effect of the microbiome on egg carotenoid investment, nestling development and oxidative cost of reproduction and thus highlights the major effect that the microbiome may have on the evolution of host life-history strategies.Functional Ecology 01/2015; DOI:10.1111/1365-2435.12404 · 4.86 Impact Factor
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ABSTRACT: Costs and benefits of the immune response have attracted considerable attention in the last years among evolutionary biologists. Given the cost of parasitism, natural selection should favor individuals with the most effective immune defenses. Nevertheless, there exists huge variation in the expression of immune effectors among individuals. To explain this apparent paradox, it has been suggested that an over-reactive immune system might be too costly, both in terms of metabolic resources and risks of immune-mediated diseases, setting a limit to the investment into immune defenses. Here, we argue that this view neglects one important aspect of the interaction: the role played by evolving pathogens. We suggest that taking into account the co-evolutionary interactions between the host immune system and the parasitic strategies to overcome the immune response might provide a better picture of the selective pressures that shape the evolution of immune functioning. Integrating parasitic strategies of host exploitation can also contribute to understand the seemingly contradictory results that infection can enhance, but also protect from, autoimmune diseases. In the last decades, the incidence of autoimmune disorders has dramatically increased in wealthy countries of the northern hemisphere with a concomitant decrease of most parasitic infections. Experimental work on model organisms has shown that this pattern may be due to the protective role of certain parasites (i.e., helminths) that rely on the immunosuppression of hosts for their persistence. Interestingly, although parasite-induced immunosuppression can protect against autoimmunity, it can obviously favor the spread of other infections. Therefore, we need to think about the evolution of the immune system using a multidimensional trade-off involving immunoprotection, immunopathology and the parasitic strategies to escape the immune response.03/2013; 2(1):71-91. DOI:10.3390/pathogens2010071
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ABSTRACT: Variation in immune defence in birds is often explained either by external factors such as food availability and disease pressure or by internal factors such as moult and reproductive effort. We explored these factors together in one sampling design by measuring immune activity over the time frame of the moulting period of Arctic-breeding barnacle geese (Branta leucopsis). We assessed baseline innate immunity by measuring levels of complement-mediated lysis and natural antibody-mediated agglutination together with total and differential leukocyte counts. Variation in immune activity during moult was strongly associated with calendar date and to a smaller degree with the growth stage of wing feathers. We suggest that the association with calendar date reflected temporal changes in the external environment. This environmental factor was further explored by comparing the immune activity of geese in the Arctic population with conspecifics in the temperate climate zone at comparable moult stages. In the Arctic environment, which has a lower expected disease load, geese exhibited significantly lower values of complement-mediated lysis, their blood contained fewer leukocytes, and levels of phagocytic cells and reactive leukocytes were relatively low. This suggests that lower baseline immune activity could be associated with lower disease pressure. We conclude that in our study species, external factors such as food availability and disease pressure have a greater effect on temporal variation of baseline immune activity than internal factors such as moult stage.PLoS ONE 12/2014; DOI:10.1371/journal.pone.0114812 · 3.53 Impact Factor