Effect of the administration of growth-hormone-producing lymphocytes on weight gain and immune function in dwarf mice

Academic Article

Abstract

  • Our previous work has shown that cells of the immune system produce a growth hormone (GH) molecule similar to that secreted by the pituitary. In the present studies, we evaluated the possibility that normal spleen cells producing GH transferred to dwarf mice could stimulate their growth. The results showed that normal spleen cells alone or spleen cells treated with growth- hormone-releasing hormone (GHRH) did not appear to significantly stimulate the growth of dwarf mice. Spleen cells activated in vitro with concanavalin A or lipopolysaccharide and then transferred to dwarf mice, or thymus cells alone, were also without effect, whereas GH alone stimulated growth as expected. Serum levels of insulin-like growth factor-I (IGF-I) and IGF-I liver RNA were undetectable in control dwarf mice and dwarf mice receiving spleen cells, whereas serum levels of IGF-I increased after treatement of dwarf mice with GH. The immune system of dwarf mice receiving spleen cells, however, was significantly altered. Spleen cells from dwarf animals showed enhanced immunoglobulin, interleukin (IL)-6, IL-2, and interferon-γ production whereas no significant change was apparent in natural killer cell activity. Despite the absence of the pit-1 protein in dwarf mice, their spleen and thymus cells retained the ability to produce almost as much lymphocyte GH as normal. Overall, the findings support the idea that the pit-1 protein in lymphocytes of dwarf mice may not be obligatory for the expression of lymphocyte GH. Further, the transfer of spleen cells to dwarf mice appears to have an autocrine/paracrine effect on the immune system rather than a pronounced endocrine effect on the growth of dwarf mice under the conditions studied. © 1994 S. Karger AG, Basel.
  • Authors

    Published In

    Digital Object Identifier (doi)

    Pubmed Id

  • 10224254
  • Author List

  • Weigent DA; Blalock JE
  • Start Page

  • 50
  • End Page

  • 58
  • Volume

  • 1
  • Issue

  • 1