Acetylcholinesterase Monoclonal Antibody-Induced Sympathectomy: Effects on Immune Status and Acute Morphine-Induced Immunomodulation

Abstract

The present study examined the role of the sympathetic nervous system (SNS) in immunomodulation by using the acetylcholinesterase monoclonal antibody (AChE mAb)-induced sympathectomy model. As part of this investigation, the effects of AChE mAb treatment on the immune alterations produced by acute morphine treatment also were explored. Experimental rats received tail vein injections of murine monoclonal IgG2b antibodies against rat brain acetylcholinesterase, which produce a destruction of cholinergic, sympathetic preganglionic neurons and a resultant decrease in sympathetic activity. Control rats received tail vein injections of murine IgG antibodies, which do not affect sympathetic preganglionic neurons or sympathetic activity. One week after antibody treatment, rats received a subcutaneous injection of 15 mg/kg morphine or the saline vehicle. One hour after the morphine or saline injections, rats were sacrificed and immune assays were conducted. AChE mAb treatment increased the mitogen-stimulated proliferation of splenic T cells and interleukin-2 (IL-2) production by stimulated splenocytes, indicating that these immune measures are sensitive to the AChE mAb-induced alteration in sympathetic function. Treatment with AChE mAb did not alter the mitogen-stimulated proliferation of splenic B cells or blood T cells, splenic natural killer (NK) cell activity, or the production of interferon-γ (IFN-γ) by stimulated splenocytes, indicating that these immune measures are relatively insensitive to the AChE mAb-induced alteration in sympathetic activity. The AChE mAb-induced alteration in sympathetic activity did not affect the suppressive effects of acute morphine treatment on the mitogen-stimulated proliferative response of splenic T and B cells and blood T cells, splenic NK cell activity, and the production of IFN-γ and IL-2 by stimulated splenocytes.