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Peer-reviewed veterinary case report

Biological response of chickens (Gallus gallus domesticus) induced by corticosterone and a bacterial endotoxin.

Journal:
Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology
Year:
2008
Authors:
Shini, Shaniko et al.
Affiliation:
School of Animal Studies · Australia

Abstract

Experiments were conducted with chickens exposed to corticosterone and lipopolysaccharide (LPS) from Escherichia coli, with the aim of evaluating and differentiating their effects on endocrine, metabolic and immune response. Both, corticosterone and LPS significantly elevated plasma corticosterone concentrations and increased heterophil to lymphocyte (H/L) ratios 1 h, 3 h and 24 h post-treatments. Repeated exposure to corticosterone caused a prolonged elevation of plasma corticosterone concentration and H/L ratio. Data on blood metabolites demonstrated that corticosterone stimulated hyperglycaemia, hypercholesterolemia and hypertriglyceridemia. In contrast, LPS induced hypocholesterolemia and hypotriglyceridemia at 24 h post-injection. Weight gain and relative weight of the spleen and bursa were reduced in chickens treated with corticosterone. The LPS did not show any significant effect on weekly weight gain, but stimulated an increase in the relative weight of the spleen. Corticosterone initially stimulated antibody responsiveness to infectious bronchitis virus (IBV) vaccination, but thereafter the titres decreased. This was in contrast to LPS which depressed the antibody titre to IBV vaccination. It was concluded that the biological response of chickens induced by corticosterone could be differed from the response to LPS. The major difference occurred in metabolic, growth and immune activities. It appears that, both corticosterone and LPS differently alter physiological, metabolic and immunological responses of chickens through an activation of different molecular components (cytokines and chemokines) and neuroendocrine-immune network systems.

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Original publication: https://pubmed.ncbi.nlm.nih.gov/18024213/