Hemmick L M, Bidlack J M
Department of Pharmacology, University of Rochester, School of Medicine and Dentistry, NY 14642.
J Neuroimmunol. 1990 Sep-Oct;29(1-3):239-48. doi: 10.1016/0165-5728(90)90167-l.
beta-Endorphin 1-31 and several structurally related peptides were tested for their ability to alter mitogen-induced T cell proliferation. Rat beta-endorphin 1-31 and human beta-endorphin 1-27 increased phytohemagglutinin (PHA)-induced [3H]thymidine incorporation into rat lymph node cells. However, when PHA-induced proliferation was suppressed by the inclusion of prostaglandin E1 (PGE1), human beta-endorphin 1-31 and a number of structurally similar peptides, including some peptides that did not alter mitogen-induced proliferation, significantly reduced the PGE1 inhibition of PHA-stimulated T cell proliferation. Although the N-terminus of beta-endorphin was necessary for potency, inclusion of the opioid antagonist naloxone together with beta-endorphin 1-31 did not alter the blockage of PGE1 inhibition of PHA-induced proliferation caused by beta-endorphin. The inhibition of mitogen-stimulated proliferation by either cholera toxin or forskolin, two additional compounds that like PGE1 also elevate cyclic AMP levels, was not blocked by beta-endorphin. Verapamil suppression of proliferation was not modified by beta-endorphin, indicating that the beta-endorphin stimulatory effect was probably not due to Ca2+ influx through verapamil-sensitive Ca2+ channels. These data suggest that beta-endorphin, acting through a nonopioid beta-endorphin receptor, may modulate immunocompetence by stimulating T cell proliferation and by counteracting the inhibitory effects of PGE1.
