TY - JOUR
T1 - Evidence for the involvement of β-adrenergic receptors in conditioned immunomodulation
AU - Luecken, Linda J.
AU - Lysle, Donald T.
N1 - Funding Information:
We are grateful to Elizabeth H. Bennett and Kimberly A. Maslonek for their technical assistance on this project. This work was supported by a grant to D.T.L. from the National Institute of Mental Health (MH46284).
PY - 1992/6
Y1 - 1992/6
N2 - This study investigates the role of β-adrenergic receptors in the immunomodulatory effects of a conditioned aversive stimulus (CS). A CS is an environmental event that is not inherently aversive, but acquires aversive properties through pairings with a stimulus such as electric shock. This study evaluated the effects of administration of the β1-receptor selective antagonist atenolol, and the β2-receptor antagonist ICI 118,551 on conditioned immune alterations. Administration of either antagonist prior to presentation of the CS resulted in a dose-dependent attenuation of the CS-induced suppression of splenic T-cell proliferative response to concanavalin. A, phytohemagglutinin, and the combination of ionomycin/phorbol-myristate-acetate. Furthermore, both antagonists dose-dependently attenuated the CS-induced suppression of γ-interferon production by concanavalin-A (ConA)-stimulated splenocytes. In contrast, neither antagonist significantly attenuated the CS-induced suppression of the B-cell mitogenic response to LPS, interleukin-2 production, natural killer cell activity, or mitogenic responsiveness of blood lymphocytes. Thus it is likely that multiple mechanisms are involved in CS-induced immune alterations and these results clearly implicate β1 and β2-adrenergic receptors in a subset of immunomodulatory effects.
AB - This study investigates the role of β-adrenergic receptors in the immunomodulatory effects of a conditioned aversive stimulus (CS). A CS is an environmental event that is not inherently aversive, but acquires aversive properties through pairings with a stimulus such as electric shock. This study evaluated the effects of administration of the β1-receptor selective antagonist atenolol, and the β2-receptor antagonist ICI 118,551 on conditioned immune alterations. Administration of either antagonist prior to presentation of the CS resulted in a dose-dependent attenuation of the CS-induced suppression of splenic T-cell proliferative response to concanavalin. A, phytohemagglutinin, and the combination of ionomycin/phorbol-myristate-acetate. Furthermore, both antagonists dose-dependently attenuated the CS-induced suppression of γ-interferon production by concanavalin-A (ConA)-stimulated splenocytes. In contrast, neither antagonist significantly attenuated the CS-induced suppression of the B-cell mitogenic response to LPS, interleukin-2 production, natural killer cell activity, or mitogenic responsiveness of blood lymphocytes. Thus it is likely that multiple mechanisms are involved in CS-induced immune alterations and these results clearly implicate β1 and β2-adrenergic receptors in a subset of immunomodulatory effects.
KW - Atenolol
KW - Conditioned aversive stimulus
KW - ICI 118,551
KW - Immunomodulation
KW - β-Adrenergic receptor
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U2 - 10.1016/0165-5728(92)90014-C
DO - 10.1016/0165-5728(92)90014-C
M3 - Article
C2 - 1351060
AN - SCOPUS:0026632677
SN - 0165-5728
VL - 38
SP - 209
EP - 219
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 3
ER -