The periparturient relaxation of immunity in Merino ewes infected with Trichostrongylus colubriformis: endocrine and body compositional responses.
The temporal association between the periparturient rise in worm egg count of grazing Merino ewes to infection with Trichostrongylus colubriformis and the underlying causal mechanisms was investigated in an experiment that incorporated two levels of pregnancy (pregnant or unmated), two levels of infection (infected with 6000 T. colubriformis L(3)/week or uninfected) and, following lambing, three levels of lactation (non-lactating/"dry", early-weaned 2 days after parturition, or suckled). In addition to parasitological and host immune responses reported in a previous paper (Beasley et al., 2010), a range of endocrine and body compositional changes were monitored from day -50 to day 42, relative to the midpoint of lambing (day 0). By day -19, pregnant ewes had begun to mobilise fat and eye muscle, and after 42 days of suckling had lost 31% and 8%, respectively, of their existing depots. In comparison to non-pregnant (dry) ewes, the endocrine profiles of late-pregnant ewes were characterised by low levels of cortisol and prolactin and high levels of progesterone and oestradiol. Lactating ewes had lower levels of cortisol and leptin and higher levels of prolactin compared to both dry and early-weaned ewes. The mobilisation of fat and protein reserves throughout lactation in suckled ewes was closely associated with leptin and cortisol profiles, and provided strong evidence of an underlying nutritional basis for the periparturient relaxation of immunity. Both leptin and cortisol concentrations were also associated with both parasite burden and the immune status of the ewe. It is suggested that lower blood cortisol levels in suckled ewes contribute to a Th1 biased immune response that leads to an increased susceptibility to gastrointestinal nematodes. The results provide a detailed characterisation of the physiology underlying the periparturient relaxation of immunity to T. colubriformis, from which further investigations will aim to expose potential causal factors.
Beasley
A M
AM
Australian Sheep Industry CRC, CJ Hawkins Homestead, School of Environmental and Rural Science, University of New England, Armidale, NSW, Australia. beasleyab@bigpond.com
Kahn
L P
LP
Windon
R G
RG
D000273:Adipose Tissue / Q000276:immunology; D000818:Animals; D001823:Body Composition / Q000276:immunology*; D001835:Body Weight / Q000276:immunology; D004703:Endocrine System / Q000276:immunology*; D005260:Female; D006728:Hormones / Q000097:blood; D009132:Muscles / Q000276:immunology; D049590:Postpartum Period; D011247:Pregnancy; D012756:Sheep; D012757:Sheep Diseases / Q000276:immunology*; D014253:Trichostrongylosis / Q000276:immunology / Q000662:veterinary*; D014254:Trichostrongylus
D006728:Hormones