K. Fecho et al., ACETYLCHOLINESTERASE MONOCLONAL ANTIBODY-INDUCED SYMPATHECTOMY - EFFECTS ON IMMUNE STATUS AND ACUTE MORPHINE-INDUCED IMMUNOMODULATION, Brain, behavior, and immunity, 11(3), 1997, pp. 167-184
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 inve
stigation, 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 antibod
ies against rat brain acetylcholinesterase, which produce a destructio
n of cholinergic, sympathetic preganglionic neurons and a resultant de
crease in sympathetic activity. Control rats received tail vein inject
ions of murine IgG antibodies, which do not affect sympathetic pregang
lionic neurons or sympathetic activity. One week after antibody treatm
ent, rats received a subcutaneous injection of 15 mg/kg morphine or th
e saline vehicle. One hour after the morphine or saline injections, ra
ts were sacrificed and immune assays were conducted. AChE mAb treatmen
t increased the mitogen-stimulated proliferation of splenic T cells an
d interleukin-2 (IL-2) production by stimulated splenocytes, indicatin
g that these immune measures are sensitive to the AChE mAb-induced alt
eration in sympathetic function. Treatment with AChE mAb did not alter
the mitogen-stimulated proliferation of splenic B cells or blood T ce
lls, splenic natural killer (NK) cell activity, or the production of i
nterferon-gamma (IFN-gamma) by stimulated splenocytes, indicating that
these immune measures are relatively insensitive to the AChE mAb-indu
ced alteration in sympathetic activity. The AChE mAb-induced alteratio
n in sympathetic activity did not affect the suppressive effects of ac
ute morphine treatment on the mitogen-stimulated proliferative respons
e of splenic T and B cells and blood T cells, splenic NK cell activity
, and the production of IFN-gamma, and IL-2 by stimulated splenocytes.
(C) 1997 Academic Press.