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United States Department of Agriculture

Agricultural Research Service

Research Project: ENHANCING ANIMAL WELL-BEING, IMMUNOCOMPETENCE, AND PERFORMANCE IN SWINE AND BEEF CATTLE Title: Insulin-like growth factor-1 attenuates glucocorticoid suppression of pig lymphocyte function

Authors
item Collier, Chad
item Welsh, Thomas -
item Carroll, Jeffery
item Laurenz, Jamie -

Submitted to: Food and Agricultural Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 16, 2011
Publication Date: December 1, 2011
Citation: Collier, C.T., Welsh Jr, T.H., Carroll, J.A., Laurenz, J.C. 2011. Insulin-like growth factor-1 attenuates glucocorticoid suppression of pig lymphocyte function. Food and Agricultural Immunology. 22(4):311-323.

Interpretive Summary: The present study determined the effects of a synthetic stress hormone (dexamethasone, DEX) and a growth hormone (IGF-1) on immune cell function. Specifically, immune cells were stimulated in vitro with an infectious agent and subsequent cell proliferation and antibody (IgM) production were analyzed. Blood samples were obtained from male, crossbred pigs (45 days of age, n=3/experiment) and blood immune cells were isolated. Cells were stimulated with the infectious agents Concanavalin A (ConA) and Pokeweed Mitogen (PWM) combined with DEX and/or IGF-1. ConA and PWM caused increases in both immune cell proliferation and IgM production. Dexamethasone suppressed immune cell proliferation and IgM production in response to submaximal levels of ConA and PWM. However, DEX was unable to suppress IgM production at concentrations of ConA and PWM which induced maximal IgM production. In the absence of the infectious agents, IGF-1 induced increases in cell proliferation, but did not affect IgM production. The addition of IGF-1 enhanced both cell proliefation and IgM production in the presence of ConA. However, IGF-1 did not affect cell proliferation or IgM production in the presence of PWM. IGF-1 diminished the suppressive effects of DEX on PWM-induced IgM production. Collectively, these results demonstrate that IGF-1 can enhance the response of immune cells to infection and reduce the suppressive effects of stress-related hormones. In addition, the ability of IGF-1 to modulate immune cell function in the presence of ConA, but not PWM, suggest that the effects of IGF-1 on proliferation and IgM production were primarily mediated through immune cell stimulation.

Technical Abstract: The present study determined the effects of a synthetic glucocorticoid (dexamethasone, DEX) and IGF-1 on mitogen-induced proliferation and immunoglobulin (Ig) production by pig lymphocytes in vitro. Blood samples were obtained via jugular venipuncture from male, crossbred pigs (45 days of age, n=3/experiment) and peripheral blood lymphocytes isolated. Cells were stimulated with Concanavalin A (ConA), Pokeweed Mitogen (PWM), dexamethasone (DEX), and/or recombinant human IGF-1. ConA and PWM induced dose-dependent increases in both lymphoproliferation and IgM production. Although not affecting basal value, DEX dose-dependently suppressed lymphoproliferation and IgM production in response to submaximal concentrations of ConA and PWM. However, DEX was unable to suppress IgM production at concentrations of ConA and PWM which induced maximal IgM production. In the absence of mitogens, IGF-1 induced dose-dependent increases in lymphoproliferation, but did not affect IgM production. The addition of IGF-1 enhanced both lymphoproliferation and IgM production in the presence of ConA. However, IGF-1 did not affect lymphoproliferation or IgM production in the presence of PWM. IGF-1 attenuated the suppressive effects of DEX on PWM-induced IgM production. Collectively, these results demonstrate that IGF-1 can enhance the response of lymphocytes to antigenic challenge and reduce the suppressive effects of glucocorticoids. In addition, the ability of IGF-1 to modulate lymphocyte function in the presence of ConA, but not PWM, suggests that the effects of IGF-1 on proliferation and immunoglobulin production were primarily mediated through T lymphocyte stimulation.

Last Modified: 10/24/2014
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