Related Experiment Videos
Insulin-like growth factor-I enhances immune response in dexamethasone-treated or surgically stressed rats maintained
P S Hinton1, C A Peterson, H C Lo
1Department of Nutritional Sciences, University of Wisconsin-Madison 53706, USA.
Background:
New evidence suggests that insulin-like growth factor-I (IGF-I) is an important regulator of immune response. Our objective was to determine the effects of IGF-I on immune response during total parenteral nutrition (TPN) using two stress models.
Methods:
Male, Sprague-Dawley rats (230 to 250 g) were given TPN with or without coinfusion of recombinant human IGF-I (800 micrograms/d for 6 days) and subjected to either dexamethasone, a synthetic glucocorticoid, or surgical stress, in the form of a midline abdominal incision. In the dexamethasone model, immune response was assessed by total cellularity of the thymus and spleen, in vitro assays of lymphocyte proliferation, and interleukin 6 (IL-6) production, and concentrations of IL-6 and tumor necrosis factor alpha (TNF-alpha) in serum. In the surgical model, flow cytometry was used to identify and quantify splenic populations of T and B lymphocytes and macrophages.
Results:
In rats immunosuppressed by dexamethasone, IGF-I infusion increased mitogen-induced proliferation of thymocytes, but did not alter cellularity in the thymus; enhanced proliferation and IL-6 production in peripheral blood mononuclear cells following treatment with concanavalin A or lipopolysaccharide; and reduced the serum concentration of IL-6, but not TNF-alpha. In surgically stressed rats, IGF-I infusion restored the splenic populations of immature and mature B lymphocytes, which were decreased by TPN.
Conclusions:
our data demonstrate that IGF-1 enhances immune response during TPN in rats.