Costs of immunity and their role in the range expansion of the house sparrow in Kenya.

There are at least two reasons to study traits that mediate successful range expansions. First, dispersers will found new populations and thus impact the distribution and evolution of species. Second, organisms moving into new areas will influence the fate of resident communities, directly competing with or indirectly affecting residents by spreading non-native or spilling-back native parasites. The success of invaders in new areas is likely mediated by a counterbalancing of costly traits. In new areas where threats are comparatively rare, individuals that grow rapidly and breed prolifically should be at an advantage. High investment in defenses should thus be disfavored. In the present study, we compared the energetic, nutritional and collateral damage costs of an inflammatory response among Kenyan house sparrow (Passer domesticus) populations of different ages, asking whether costs were related to traits of individuals from three different capture sites. Kenya is among the world's most recent range expansions for this species, and we recently found that the expression of Toll-like receptors (TLRs), leukocyte receptors that instigate inflammatory responses when bound to microbial elements, was related to the range expansion across the country. Here, we found (contrary to our expectations) that energetic and nutritional costs of inflammation were higher, but damage costs were lower, in range-edge compared with core birds. Moreover, at the individual level, TLR-4 expression was negatively related to commodity costs (energy and a critical amino acid) of inflammation. Our data thus suggest that costs of inflammation, perhaps mediated by TLR expression, might mitigate successful range expansions.

Short-Term Sleep Loss Alters Cytokine Gene Expression in Brain and Peripheral Tissues and Increases Plasma Corticosterone of Zebra Finch (Taeniopygia guttata).

Lack of sleep incurs physiological costs that include increased inflammation and alterations in the hypothalamic-pituitary-adrenal axis. Specifically, sleep restriction or deprivation leads to increased pro-inflammatory cytokine expression and elevated glucocorticoids in rodent models, but whether birds exact similar costs is unknown. In this study, we examined whether zebra finch (Taeniopygia guttata), an avian model species, exhibits physiological costs of sleep loss by using a novel automated sleep fragmentation/deprivation method, wherein a horizontal wire sweeps across a test cage to disrupt sleep every 120 s. We measured pro-inflammatory (IL-1ß and IL-6) and anti-inflammatory (IL-10) cytokine gene expression in the periphery (fat, liver, spleen, and heart) and brain (hypothalamus, hippocampus, and apical hyperpallium) of captive finches after 12 h of exposure to a moving or stationary (control) bar during the night or the day. Plasma corticosterone, body mass, and behavioral profiles were also assessed. We predicted that birds undergoing sleep loss would exhibit elevated pro-inflammatory and reduced anti-inflammatory gene expression in brain and peripheral tissues compared with control birds. In addition, we predicted an increase in plasma corticosterone levels after sleep loss. As predicted, sleep loss increased pro-inflammatory gene expression, specifically in adipose tissue (IL-6), spleen (IL-1), and hippocampus (IL-6), but a decrease in anti-inflammatory expression (IL-10) was not detected. However, sleep loss elevated baseline concentrations of plasma corticosterone. Taken together, these results suggest that a diurnal songbird is sensitive to the costs of sleep loss.