RESUMEN
Empirical data relating body mass to immune defence against infections remain limited. Although the metabolic theory of ecology predicts that larger organisms would have weaker immune responses, recent studies have suggested that the opposite may be true. These discoveries have led to the safety factor hypothesis, which proposes that larger organisms have evolved stronger immune defences because they carry greater risks of exposure to pathogens and parasites. In this study, we simulated sepsis by exposing blood from nine primate species to a bacterial lipopolysaccharide (LPS), measured the relative expression of immune and other genes using RNAseq, and fitted phylogenetic models to determine how gene expression was related to body mass. In contrast to non-immune-annotated genes, we discovered hypermetric scaling in the LPS-induced expression of innate immune genes, such that large primates had a disproportionately greater increase in gene expression of immune genes compared to small primates. Hypermetric immune gene expression appears to support the safety factor hypothesis, though this pattern may represent a balanced evolutionary mechanism to compensate for lower per-transcript immunological effectiveness. This study contributes to the growing body of immune allometry research, highlighting its importance in understanding the complex interplay between body size and immunity over evolutionary timescales.
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Primates , Sepsis , Transcriptoma , Animales , Sepsis/veterinaria , Sepsis/inmunología , Lipopolisacáridos , Inmunidad Innata , Tamaño Corporal , FilogeniaRESUMEN
For most of its history, immunology has sought to control environmental variation to establish genetic causality. As with all biological traits though, variation among individuals arises by three broad pathways: genetic (G), environmental (E), and the interactive between the two (GxE); and immunity is no different. Here, we review the value of applying the evolutionary frameworks of phenotypic plasticity and reaction norms to immunology. Because standardized laboratory environments are vastly different from the conditions under which populations evolved, we hypothesize that immunology might presently be missing important phenotypic variation and even focusing on dysregulated molecular and cellular processes. Modest adjustments to study designs could make model organism immunology more productive, reproducible, and reflective of human physiology.
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Adaptación Fisiológica , Evolución Biológica , Variación Genética , Humanos , FenotipoRESUMEN
When organisms move into new areas, they are likely to encounter novel food resources. Even if they are nutritious, these foods can also be risky, as they might be contaminated by parasites. The behavioural immune system of animals could help them avoid the negative effects of contaminated resources, but our understanding of behavioural immunity is limited, particularly whether and how behavioural immunity interacts with physiological immunity. Here, we asked about the potential for interplay between these two traits, specifically how the propensity of an individual house sparrow (Passer domesticus) to take foraging risks was related to its ability to regulate a key facet of its immune response to bacterial pathogens. Previously, we found that sparrows at expanding geographic range edges were more exploratory and less risk-averse to novel foods; in those same populations, birds tended to over-express Toll-like receptor 4 (TLR4), a pattern-recognition receptor that distinguishes cell-wall components of Gram-negative bacteria, making it the major sensor of potentially lethal gut microbial infections including salmonellosis. When we investigated how birds would respond to a typical diet (i.e., mixed seeds) spiked with domesticated chicken faeces, birds that expressed more TLR4 or had higher epigenetic potential for TLR4 (more CpG dinucleotides in the putative gene promoter) ate more food, spiked or not. Females expressing abundant TLR4 were also willing to take more foraging risks and ate more spiked food. In males, TLR4 expression was not associated with risk-taking. Altogether, our results indicate that behaviour and immunity covary among individual house sparrows, particularly in females where those birds that maintain more immune surveillance also are more disposed to take foraging risks.
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Epigénesis Genética , Conducta Alimentaria , Gorriones , Animales , Gorriones/inmunología , Femenino , Conducta Alimentaria/fisiología , Receptor Toll-Like 4/genética , Receptor Toll-Like 4/metabolismo , Asunción de Riesgos , Expresión Génica , Pollos/inmunología , Masculino , Conducta Animal/fisiologíaRESUMEN
As a highly successful introduced species, house sparrows (Passer domesticus) respond rapidly to their new habitats, generating phenotypic patterns across their introduced range that resemble variation in native regions. Epigenetic mechanisms likely facilitate the success of introduced house sparrows by aiding particular individuals to adjust their phenotypes plastically to novel conditions. Our objective here was to investigate patterns of DNA methylation among populations of house sparrows at a broad geographic scale that included different introduction histories: invading, established, and native. We defined the invading category as the locations with introductions less than 70 years ago and the established category as the locations with greater than 70 years since introduction. We screened DNA methylation among individuals (nâ =â 45) by epiRADseq, expecting that variation in DNA methylation among individuals from invading populations would be higher when compared with individuals from established and native populations. Invading house sparrows had the highest variance in DNA methylation of all three groups, but established house sparrows also had higher variance than native ones. The highest number of differently methylated regions were detected between invading and native populations of house sparrow. Additionally, DNA methylation was negatively correlated to time-since introduction, which further suggests that DNA methylation had a role in the successful colonization's of house sparrows.
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Metilación de ADN , Gorriones , Humanos , Animales , Gorriones/genética , Epigénesis Genética , EcosistemaRESUMEN
AbstractTerrestrial mammals span seven orders of magnitude in body size, ranging from the <2-g Etruscan pygmy shrew (Suncus etruscus) to the >3,900-kg African elephant (Loxodonta africana). Although body size profoundly affects the behavior, physiology, ecology, and evolution of species, how investment in functional immune defenses changes with body size across species is unknown. Here, we (1) developed a novel 12-point dilution curve approach to describe and compare antibacterial capacity against three bacterial species among >160 terrestrial species of mammals and (2) tested published predictions about the scaling of immune defenses. Our study focused on the safety factor hypothesis, which predicts that broad, early-acting immune defenses should scale hypermetrically with body mass. However, our three statistical approaches demonstrated that antibacterial activity in sera across mammals exhibits isometry; killing capacity did not change with body size across species. Intriguingly, this result indicates that the serum of a large mammal is less hospitable to bacteria than would be predicted by its metabolic rates. In other words, if metabolic rates underlie the rates of physiological reactions as postulated by the metabolic theory of ecology, large species should have disproportionately lower antibacterial capacity than small species, but they do not. These results have direct implications for effectively modeling the evolution of immune defenses and identifying potential reservoir hosts of pathogens.
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Mamíferos , Animales , Mamíferos/fisiología , Tamaño CorporalRESUMEN
Animals encounter many novel and unpredictable challenges when moving into new areas, including pathogen exposure. Because effective immune defenses against such threats can be costly, plastic immune responses could be particularly advantageous, as such defenses can be engaged only when context warrants activation. DNA methylation is a key regulator of plasticity via its effects on gene expression. In vertebrates, DNA methylation occurs exclusively at CpG dinucleotides and, typically, high DNA methylation decreases gene expression, particularly when it occurs in promoters. The CpG content of gene regulatory regions may therefore represent one form of epigenetic potential (EP), a genomic means to enable gene expression and hence adaptive phenotypic plasticity. Non-native populations of house sparrows (Passer domesticus) - one of the world's most cosmopolitan species - have high EP in the promoter of a key microbial surveillance gene, Toll-like receptor 4 (TLR4), compared with native populations. We previously hypothesized that high EP may enable sparrows to balance the costs and benefits of inflammatory immune responses well, a trait critical to success in novel environments. In the present study, we found support for this hypothesis: house sparrows with high EP in the TLR4 promoter were better able to resist a pathogenic Salmonella enterica infection than sparrows with low EP. These results support the idea that high EP contributes to invasion and perhaps adaptation in novel environments, but the mechanistic details whereby these organismal effects arise remain obscure.
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Salmonella enterica , Gorriones , Animales , Receptor Toll-Like 4/genética , Salmonella enterica/genética , Gorriones/fisiología , Epigénesis GenéticaRESUMEN
Variation in DNA methylation is associated with many ecological and life history traits, including niche breadth and lifespan. In vertebrates, DNA methylation occurs almost exclusively at "CpG" dinucleotides. Yet, how variation in the CpG content of the genome impacts organismal ecology has been largely overlooked. Here, we explore associations between promoter CpG content, lifespan and niche breadth among 60, amniote vertebrate species. The CpG content of 16 functionally relevant gene promoters was strongly, positively associated with lifespan in mammals and reptiles, but was not related to niche breadth. Possibly, by providing more substrate for CpG methylation to occur, high promoter CpG content extends the time taken for deleterious, age-related errors in CpG methylation patterns to accumulate, thereby extending lifespan. The association between CpG content and lifespan was driven by gene promoters with intermediate CpG enrichment-those known to be predisposed to regulation by methylation. Our findings provide novel support for the idea that high CpG content has been selected for in long-lived species to preserve the capacity for gene expression regulation by CpG methylation. Intriguingly, promoter CpG content was also dependent on gene function in our study; immune genes had on average 20% less CpG sites than metabolic- and stress-related genes.
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Longevidad , Vertebrados , Animales , Longevidad/genética , Vertebrados/genética , Metilación de ADN , Mamíferos/genética , Biomarcadores , Epigénesis GenéticaRESUMEN
AbstractDuring range expansions, organisms can use epigenetic mechanisms to adjust to conditions in novel areas by altering gene expression and enabling phenotypic plasticity. Here, we predicted that the number of CpG sites within the genome, one form of epigenetic potential, would be important for successful range expansions because DNA methylation can modulate gene expression and, consequently, plasticity. We asked how the number of CpG sites and DNA methylation varied across five locations in the â¼70-year-old Kenyan house sparrow (Passer domesticus) range expansion. We found that the number of CpG sites was highest toward the vanguard of the invasion and decreased toward the range core. Analysis suggests that this pattern may have been driven by selection, favoring birds with more CpG sites at the range edge. However, we cannot rule out other processes, including nonrandom gene flow. Additionally, DNA methylation did not change across the range expansion, nor was it more variable. We hypothesize that as new areas are colonized, epigenetic potential may be selectively advantageous early but eventually be replaced by less plastic and perhaps genetically canalized traits as populations adapt to local conditions. Although further work is needed on epigenetic potential, this form (CpG number) appears to be a promising mechanism to investigate as a driver of expansions via capacitated phenotypic plasticity in other natural and anthropogenic range expansions.
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Gorriones , Animales , Gorriones/genética , Metilación de ADN , Kenia , Epigénesis Genética , PlásticosRESUMEN
Emerging infectious diseases (EIDs) present global health threats, and their emergences are often linked to anthropogenic change. Artificial light at night (ALAN) is one form of anthropogenic change that spans beyond urban boundaries and may be relevant to EIDs through its influence on the behaviour and physiology of hosts and/or vectors. Although West Nile virus (WNV) emergence has been described as peri-urban, we hypothesized that exposure risk could also be influenced by ALAN in particular, which is testable by comparing the effects of ALAN on prevalence while controlling for other aspects of urbanization. By modelling WNV exposure among sentinel chickens in Florida, we found strong support for a nonlinear relationship between ALAN and WNV exposure risk in chickens with peak WNV risk occurring at low ALAN levels. Although our goal was not to discern how ALAN affected WNV relative to other factors, effects of ALAN on WNV exposure were stronger than other known drivers of risk (i.e. impervious surface, human population density). Ambient temperature in the month prior to sampling, but no other considered variables, strongly influenced WNV risk. These results indicate that ALAN may contribute to spatio-temporal changes in WNV risk, justifying future investigations of ALAN on other vector-borne parasites.
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Fiebre del Nilo Occidental , Virus del Nilo Occidental , Animales , Pollos , Contaminación Ambiental , Florida/epidemiología , Humanos , Fiebre del Nilo Occidental/epidemiología , Fiebre del Nilo Occidental/veterinariaRESUMEN
The hypothalamic-pituitary-adrenal (HPA) axis and its end products, the glucocorticoids, are critical to responding appropriately to stressors. Subsequently, many studies have sought relationships between glucocorticoids and measures of health or fitness, but such relationships are at best highly context dependent. Recently, some endocrinologists have started to suggest that a focus on HPA flexibility, the ability of an individual to mount appropriate responses to different stressors, could be useful. Here, we tested the hypothesis that expression of FKBP5, a cochaperone in the glucocorticoid receptor complex, is a simple and reliable proxy of HPA flexibility in a wild songbird, the house sparrow (Passer domesticus). We quantified HPA flexibility in a novel way, using guidance from research on heart rhythm regulation. As predicted, we found that adult sparrows with low stress-induced FKBP5 expression in the hypothalamus exhibited high HPA flexibility. Moreover, low FKBP5 expression was associated with greater exploratory disposition and were better at maintaining body mass under stressful conditions. Altogether, these results suggest that FKBP5 may be important in the regulation of HPA flexibility, potentially affecting how individuals cope with natural and anthropogenic adversity.
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Gorriones , Animales , Corticosterona , Femenino , Glucocorticoides , Humanos , Sistema Hipotálamo-Hipofisario , Masculino , Sistema Hipófiso-SuprarrenalRESUMEN
Epigenetic mechanisms may play a central role in mediating phenotypic plasticity, especially during range expansions, when populations face a suite of novel environmental conditions. Individuals may differ in their epigenetic potential (EP; their capacity for epigenetic modifications of gene expression), which may affect their ability to colonize new areas. One form of EP, the number of CpG sites, is higher in introduced house sparrows (Passer domesticus) than in native birds in the promoter region of a microbial surveillance gene, Toll-like Receptor 4 (TLR4), which may allow invading birds to fine-tune their immune responses to unfamiliar parasites. Here, we compared TLR4 gene expression from whole blood, liver and spleen in house sparrows with different EP, first challenging some birds with lipopolysaccharide (LPS), to increase gene expression by simulating a natural infection. We expected that high EP would predict high inducibility and reversibility of TLR4 expression in the blood of birds treated with LPS, but we did not make directional predictions regarding organs, as we could not repeatedly sample these tissues. We found that EP was predictive of TLR4 expression in all tissues. Birds with high EP expressed more TLR4 in the blood than individuals with low EP, regardless of treatment with LPS. Only females with high EP exhibited reversibility in gene expression. Further, the effect of EP varied between sexes and among tissues. Together, these data support EP as one regulator of TLR4 expression.
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Gorriones , Animales , Epigénesis Genética , Femenino , Expresión Génica , Humanos , Lipopolisacáridos/farmacología , Gorriones/genética , BazoRESUMEN
Powered flight has evolved several times in vertebrates and constrains morphology and physiology in ways that likely have shaped how organisms cope with infections. Some of these constraints probably have impacts on aspects of immunology, such that larger fliers might prioritize risk reduction and safety. Addressing how the evolution of flight may have driven relationships between body size and immunity could be particularly informative for understanding the propensity of some taxa to harbor many virulent and sometimes zoonotic pathogens without showing clinical disease. Here, we used a comparative framework to quantify scaling relationships between body mass and the proportions of two types of white blood cells - lymphocytes and granulocytes (neutrophils/heterophils) - across 63 bat species, 400 bird species and 251 non-volant mammal species. By using phylogenetically informed statistical models on field-collected data from wild Neotropical bats and from captive bats, non-volant mammals and birds, we show that lymphocyte and neutrophil proportions do not vary systematically with body mass among bats. In contrast, larger birds and non-volant mammals have disproportionately higher granulocyte proportions than expected for their body size. Our inability to distinguish bat lymphocyte scaling from birds and bat granulocyte scaling from all other taxa suggests there may be other ecological explanations (i.e. not flight related) for the cell proportion scaling patterns. Future comparative studies of wild bats, birds and non-volant mammals of similar body mass should aim to further differentiate evolutionary effects and other aspects of life history on immune defense and its role in the tolerance of (zoonotic) infections.
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Quirópteros , Animales , Aves , Tamaño Corporal , Vuelo Animal , Mamíferos , VertebradosRESUMEN
Theory predicts that body mass should affect the way organisms evolve and use immune defenses. We investigated the relationship between body mass and blood neutrophil and lymphocyte concentrations among more than 250 terrestrial mammalian species. We tested whether existing theories (e.g., protecton theory, immune system complexity, and rate of metabolism) accurately predicted the scaling of immune cell concentrations. We also evaluated the predictive power of body mass for these leukocyte concentrations compared to sociality, diet, life history, and phylogenetic relatedness. Phylogeny explained >70% of variation in both lymphocytes and neutrophils, and body mass appeared more informative than other interspecific trait variation. In the best-fit mass-only model, neutrophils scaled hypermetrically (b=0.11) with body mass, whereas lymphocytes scaled just shallow of isometrically. Extrapolating to total cell numbers, this exponent means that an African elephant circulates 13.3 million times the neutrophils of a house mouse, whereas their masses differ by only 250,000-fold. We hypothesize that such high neutrophil numbers might offset the (i) higher overall parasite exposure that large animals face and/or (ii) the higher relative replication capacities of pathogens to host cells.
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Peso Corporal/inmunología , Sistema Inmunológico/fisiología , Mamíferos/fisiología , Animales , Evolución Biológica , Mamíferos/inmunología , Modelos Biológicos , FilogeniaRESUMEN
Body mass affects many biological traits, but its impacts on immune defences are fairly unknown. Recent research on mammals found that neutrophil concentrations disproportionately increased (scaled hypermetrically) with body mass, a result not predicted by any existing theory. Although the scaling relationship for mammals might predict how leucocyte concentrations scale with body mass in other vertebrates, vertebrate classes are distinct in many ways that might affect their current and historic interactions with parasites and hence the evolution of their immune systems. Subsequently, here, we asked which existing scaling hypothesis best-predicts relationships between body mass and lymphocyte, eosinophil and heterophil concentrations-the avian functional equivalent of neutrophils-among more than 100 species of birds. We then examined the predictive power of body mass relative to life-history variation, as extensive literature indicates that the timing of key life events has influenced immune system variation among species. Finally, we ask whether avian scaling patterns differ from the patterns we observed in mammals. We found that an intercept-only model best explained lymphocyte and eosinophil concentrations among birds, indicating that the concentrations of these cell types were both independent of body mass. For heterophils, however, body mass explained 31% of the variation in concentrations among species, much more than life-history variation (4%). As with mammalian neutrophils, avian heterophils scaled hypermetrically (b= 0.19 ± 0.05), but more steeply than mammals (approx. 1.5 ×; 0.11 ± 0.03). As such, we discuss why birds might require more broadly protective cells compared to mammals of the same body size. Overall, body mass appears to have strong influences on the architecture of immune systems.
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Aves , Tamaño Corporal , Sistema Inmunológico , Animales , Evolución Biológica , Rasgos de la Historia de Vida , FilogeniaRESUMEN
The prevalence and intensity of parasites in wild hosts varies across space and is a key determinant of infection risk in humans, domestic animals and threatened wildlife. Because the immune system serves as the primary barrier to infection, replication and transmission following exposure, we here consider the environmental drivers of immunity. Spatial variation in parasite pressure, abiotic and biotic conditions, and anthropogenic factors can all shape immunity across spatial scales. Identifying the most important spatial drivers of immunity could help pre-empt infectious disease risks, especially in the context of how large-scale factors such as urbanization affect defence by changing environmental conditions. We provide a synthesis of how to apply macroecological approaches to the study of ecoimmunology (i.e. macroimmunology). We first review spatial factors that could generate spatial variation in defence, highlighting the need for large-scale studies that can differentiate competing environmental predictors of immunity and detailing contexts where this approach might be favoured over small-scale experimental studies. We next conduct a systematic review of the literature to assess the frequency of spatial studies and to classify them according to taxa, immune measures, spatial replication and extent, and statistical methods. We review 210 ecoimmunology studies sampling multiple host populations. We show that whereas spatial approaches are relatively common, spatial replication is generally low and unlikely to provide sufficient environmental variation or power to differentiate competing spatial hypotheses. We also highlight statistical biases in macroimmunology, in that few studies characterize and account for spatial dependence statistically, potentially affecting inferences for the relationships between environmental conditions and immune defence. We use these findings to describe tools from geostatistics and spatial modelling that can improve inference about the associations between environmental and immunological variation. In particular, we emphasize exploratory tools that can guide spatial sampling and highlight the need for greater use of mixed-effects models that account for spatial variability while also allowing researchers to account for both individual- and habitat-level covariates. We finally discuss future research priorities for macroimmunology, including focusing on latitudinal gradients, range expansions and urbanization as being especially amenable to large-scale spatial approaches. Methodologically, we highlight critical opportunities posed by assessing spatial variation in host tolerance, using metagenomics to quantify spatial variation in parasite pressure, coupling large-scale field studies with small-scale field experiments and longitudinal approaches, and applying statistical tools from macroecology and meta-analysis to identify generalizable spatial patterns. Such work will facilitate scaling ecoimmunology from individual- to habitat-level insights about the drivers of immune defence and help predict where environmental change may most alter infectious disease risk.
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Animales Salvajes , Parásitos , Animales , Humanos , Análisis EspacialRESUMEN
Glucocorticoid (GC) hormones are important phenotypic mediators across vertebrates, but their circulating concentrations can vary markedly. Here we investigate macroevolutionary patterning in GC levels across tetrapods by testing seven specific hypotheses about GC variation and evaluating whether the supported hypotheses reveal consistent patterns in GC evolution. If selection generally favors the "supportive" role of GCs in responding effectively to challenges, then baseline and/or stress-induced GCs may be higher in challenging contexts. Alternatively, if selection generally favors "protection" from GC-induced costs, GCs may be lower in environments where challenges are more common or severe. The predictors of baseline GCs were all consistent with supportive effects: levels were higher in smaller organisms and in those inhabiting more energetically demanding environments. During breeding, baseline GCs were also higher in populations and species with fewer lifetime opportunities to reproduce. The predictors of stress-induced GCs were instead more consistent with the protection hypothesis: during breeding, levels were lower in organisms with fewer lifetime reproductive opportunities. Overall, these patterns indicate a surprising degree of consistency in how some selective pressures shape GCs across broad taxonomic scales; at the same time, in challenging environments selection appears to operate on baseline and stress-induced GCs in distinct ways.
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Evolución Biológica , Glucocorticoides/sangre , Selección Genética , Estrés Fisiológico , Vertebrados/genética , Animales , Femenino , Masculino , Modelos Estadísticos , Vertebrados/sangreRESUMEN
Among the many anthropogenic changes that impact humans and wildlife, one of the most pervasive but least understood is light pollution. Although detrimental physiological and behavioural effects resulting from exposure to light at night are widely appreciated, the impacts of light pollution on infectious disease risk have not been studied. Here, we demonstrate that artificial light at night (ALAN) extends the infectious-to-vector period of the house sparrow (Passer domesticus), an urban-dwelling avian reservoir host of West Nile virus (WNV). Sparrows exposed to ALAN maintained transmissible viral titres for 2 days longer than controls but did not experience greater WNV-induced mortality during this window. Transcriptionally, ALAN altered the expression of gene regulatory networks including key hubs (OASL, PLBD1 and TRAP1) and effector genes known to affect WNV dissemination (SOCS). Despite mounting anti-viral immune responses earlier, transcriptomic signatures indicated that ALAN-exposed individuals probably experienced pathogen-induced damage and immunopathology, potentially due to evasion of immune effectors. A simple mathematical modelling exercise indicated that ALAN-induced increases of host infectious-to-vector period could increase WNV outbreak potential by approximately 41%. ALAN probably affects other host and vector traits relevant to transmission, and additional research is needed to advise the management of zoonotic diseases in light-polluted areas.
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Enfermedades de las Aves/virología , Reservorios de Enfermedades/veterinaria , Luz/efectos adversos , Gorriones , Fiebre del Nilo Occidental/veterinaria , Virus del Nilo Occidental/fisiología , Animales , Reservorios de Enfermedades/virología , Florida , Fiebre del Nilo Occidental/virología , Virus del Nilo Occidental/efectos de la radiaciónRESUMEN
Our previous research on range-expanding house sparrows in Kenya revealed that (i) range-edge birds released more corticosterone (CORT) in response to a stressor than range-core birds, ii) that range-edge birds were more exploratory than range-core birds, and that (iii) all birds exhibited extensive variation in genome-wide DNA methylation among individuals, regardless of their position along the range expansion. Within the hippocampus, mediators of neural plasticity such as brain-derived neurotrophic factor (BDNF), can influence and be influenced by CORT, hippocampus-associated behaviors and regulatory epigenetic modification enzymes. Here, we investigated whether individuals and populations colonizing a new geographic range, Senegal, vary in the expression of BDNF and DNA methyltransferases (DNMTs) within the hippocampus and the release of CORT in response to a stressor. DNMT expression is an important mediator of epigenetic potential, the propensity of a genome to capacitate phenotypic variation via mechanisms such as DNA methylation. We surveyed three populations across Senegal, predicting that hippocampal BDNF and DNMT expression would be highest at the range-edge, and that BDNF and DNMT would be inversely related to one another, but would each positively covary with CORT within individuals. We found a nonlinear relationship between CORT and BDNF expression within individuals. Moreover, we found that CORT positively covaried with DNMT1 expression in a more recently established population, while the reverse was true in the oldest population (i.e. at the range-core). Our study is among the first to explore whether and how variation in CORT regulation contributes to variation in mediators of neural plasticity and epigenetic potential within the hippocampus of a range-expanding vertebrate.
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Corticosterona/metabolismo , Epigenómica , Hipocampo/fisiología , Plasticidad Neuronal/fisiología , Gorriones/fisiología , Animales , Factor Neurotrófico Derivado del Encéfalo/metabolismo , ADN (Citosina-5-)-Metiltransferasa 1/metabolismo , ADN (Citosina-5-)-Metiltransferasas/metabolismo , Metilación de ADN , ADN Metiltransferasa 3A , Kenia , MasculinoRESUMEN
Glucocorticoid stress hormones, such as corticosterone (CORT), have profound effects on the behaviour and physiology of organisms, and thus have the potential to alter host competence and the contributions of individuals to population- and community-level pathogen dynamics. For example, CORT could alter the rate of contacts among hosts, pathogens and vectors through its widespread effects on host metabolism and activity levels. CORT could also affect the intensity and duration of pathogen shedding and risk of host mortality during infection. We experimentally manipulated songbird CORT, asking how CORT affected behavioural and physiological responses to a standardized West Nile virus (WNV) challenge. Although all birds became infected after exposure to the virus, only birds with elevated CORT had viral loads at or above the infectious threshold. Moreover, though the rate of mortality was faster in birds with elevated CORT compared with controls, most hosts with elevated CORT survived past the day of peak infectiousness. CORT concentrations just prior to inoculation with WNV and anti-inflammatory cytokine concentrations following viral exposure were predictive of individual duration of infectiousness and the ability to maintain physical performance during infection (i.e. tolerance), revealing putative biomarkers of competence. Collectively, our results suggest that glucocorticoid stress hormones could directly and indirectly mediate the spread of pathogens.