title: Captivity induces hyper-inflammation in the house sparrow (Passer domesticus).
abstract: Some species thrive in captivity but others exhibit extensive psychological and physiological deficits, which can be a challenge to animal husbandry and conservation as well as wild immunology. Here, we investigated whether captivity duration impacted the regulation of a key innate immune response, inflammation, of a common wild bird species, the house sparrow (Passer domesticus). Inflammation is one of the most commonly induced and fast-acting immune responses animals mount upon exposure to a parasite. However, attenuation and resolution of inflammatory responses are partly coordinated by glucocorticoid hormones, hormones that can be disregulated in captivity. Here, we tested whether captivity duration alters corticosterone regulation and hence the inflammatory response by comparing the following responses to lipopolysaccharide (LPS; a Gram-negative bacteria component that induces inflammation) of birds caught wild and injected immediately versus those held for 2 or 4 weeks in standard conditions: (1) the magnitude of leukocyte immune gene expression [the cytokines, interleukin 1β and interleukin 6, and Toll-like receptor 4 (TLR4)], (2) the rate of clearance of endotoxin, and (3) the release of corticosterone (CORT) in response to endotoxin (LPS). We predicted that captivity duration would increase baseline CORT and thus suppress gene expression and endotoxin clearance rate. However, our predictions were not supported: TLR4 expression increased with time in captivity irrespective of LPS, and cytokine expression to LPS was stronger the longer birds remained captive. Baseline CORT was not affected by captivity duration, but CORT release post-LPS occurred only in wild birds. Lastly, sparrows held captive for 4 weeks maintained significantly higher levels of circulating endotoxin than other groups, perhaps due to leakage of microbes from the gut, but exogenous LPS did not increase circulating levels over the time scale samples were collected. Altogether, captivity appears to have induced a hyper-inflammatory state in house sparrows, perhaps due to disregulation of glucocorticoids, natural microflora or both.
authors.affiliation: University of South Florida, Department of Integrative Biology, Tampa, FL 33620, USA. lmartin@cas.usf.edu
authors.forename: Lynn B
authors.initials: LB
authors.lastname: Martin
authors.forename: Laura
authors.initials: L
authors.lastname: Kidd
authors.forename: Andrea L
authors.initials: AL
authors.lastname: Liebl
authors.forename: Courtney A C
authors.initials: CA
authors.lastname: Coon
mesh_terms: D000818:Animals; D003345:Corticosterone / Q000097:blood; D005260:Female; D005431:Florida; D015870:Gene Expression; D006234:Handling, Psychological; D007249:Inflammation / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism / Q000662:veterinary*; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D007962:Leukocytes / Q000187:drug effects / Q000378:metabolism; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology; D008297:Male; D016133:Polymerase Chain Reaction; D046370:Sparrows / Q000235:genetics* / Q000276:immunology* / Q000502:physiology; D013312:Stress, Physiological; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D051197:Toll-Like Receptor 4; D003345:Corticosterone