Role of growth hormone and prolactin in regulating T-dependent immune responses and macrophage activation in aged rats
Davila, Donna Remley
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Permalink
https://hdl.handle.net/2142/20957
Description
Title
Role of growth hormone and prolactin in regulating T-dependent immune responses and macrophage activation in aged rats
Author(s)
Davila, Donna Remley
Issue Date
1989
Doctoral Committee Chair(s)
Kelley, Keith W.
Department of Study
Animal Sciences
Discipline
Animal Sciences
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biology, General
Health Sciences, Immunology
Language
eng
Abstract
Animals and humans become increasingly susceptible to infectious, arthritic, and neoplastic diseases during aging. Both growth hormone (GH) and prolactin (PRL) are important in normal immune function, and they also augment immune responses in immunocompromised and aged individuals. We previously showed that GH and PRL treatment of aged rats resulted in fully regenerated thymus glands and enhancement of certain T cell-mediated responses. The studies described here utilized primarily the aged rat model to further examine the effects of GH and PRL upon certain T cell, natural killer cell (NK), and macrophage-mediated responses.
We found that GH administration to aged rats augmented lectin-induced proliferation and NK activity. Young mice transgenic for the rat GH-metallothionein gene had higher T cell proliferation at suboptimal doses of lectins as well as more thymic epithelial cells and Hassall's corpuscles than controls. GH and PRL treatment did not enhance T cell-mediated responses in athymic nude rats. We concluded that GH augments certain T and NK cell-mediated responses in both aged and young rodents, a thymus gland is necessary for these effects, and that effects of GH are much more obvious in aged than in young rodents. We next showed that macrophages from aged rats were unable to secrete augmented amounts of superoxide anion or tumor necrosis factor in response to priming signals from interferon-$\gamma$. Implantation of ectopic pituitary grafts, which secrete both GH and PRL, restored these responses. Finally, we compared both young and aged male and female rats in four parameters of the immune response known to decline with age. Aged females had higher IL-2 synthesis and proliferation to lectins than aged males, but NK activity and antibody synthesis did not differ between aged males and females. There were no differences between young males and females in any of the four parameters measured. Hormonal differences throughout the lifespan were suggested to be responsible for the gender-associated differences in the decline of certain T cell-mediated responses during aging. These data all confirm the existence of an immune-endocrine regulatory loop, and suggest means by which impaired immune responses due to aging or other conditions may be treated in both man and animals.
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