The emergence of the epidemics in the East United States, the rapid evolution of host resistance and the persistence of immunologically naïve populations in the West can almost be considered as a natural experiment that might allow to test the following predictions: if the cost of infection is mostly due to the direct damage of the pathogen, then hosts from Arizona

(the nonexposed population) should suffer C646 nmr the most; if immunological resistance incurs costs and these constitutes the bulk of the fitness reduction in infected birds, then exposed (Alabama) hosts should suffer the most. Bonneaud et al. [73] used the same populations of house finches to measure changes in body mass intervening during the first 14 days post-infection as a proxy of infection cost. Overall, birds from the coevolved population lost more body mass than birds from the naïve population, and interestingly, the relationship between bacterial load and loss in body mass was reversed in the two populations (Figure 5a). Whereas bacterial load was negatively correlated with body mass loss in Arizona birds, indicating that most heavily infected birds lost more mass, the sign of the correlation was reversed in Alabama birds. Birds with the lowest bacterial load suffered the most intense mass reduction in Alabama. One possible interpretation of these results Selleck Natural Product Library is that body mass loss represents two different components of the cost of the infection

in the two populations: cost of immunological resistance in Alabama and cost of parasite damage in Arizona. In Idelalisib in vitro agreement with this view, the pattern of immune gene expression (indicating a protective immunity) was associated with a higher body mass loss in Alabama than in Arizona (Figure 5b). These results therefore nicely confirm in a more natural setting the findings reported for malaria parasites. Immunological

costs, whatever their nature (energetic or self-reactivity) and whatever the conferred protection (resistance or tolerance), substantially contribute to determine parasite virulence. More recently, Adelman et al. [74] explored explicitly the role played by inflammatory effectors in the resistance/tolerance of house finches experimentally infected with Mycoplasma gallisepticum. They used the same house finch populations (Alabama and Arizona) studied by Bonneaud et al. [71-73], but birds were infected with a strain of Mycoplasma isolated soon after the emergence of the epidemics. They also focused on pro- (IL-1β) and anti-inflammatory (IL-10) effectors as mediators of tolerance to infection. Interestingly, they showed that birds originating from Alabama were more tolerant to the infection (they had a better health for a given pathogen load), even though this depended on the method used to assess tolerance, than birds from Arizona. Birds from Alabama also had a lower expression of the pro-inflammatory cytokine IL-1β.