In vitro effects of Naloxone on T-lymphocyte-dependent antibacterial activity in hepatitis C virus (HCV) infected patients and in inflammatory bowel disease (IBD) patients

Naloxone acts as an opioid antagonist, displacing opioid drugs from cellula r receptors. Among opioid substances, P-endorphins are able to bind to seve ral cell receptors, even including those expressed by immune cells. In this respect, evidence has been provided that in the course of viral infections , as well as in patients with ulcerative colitis high levels of beta -endor phins are detectable. Here, peripheral blood lymphocytes (PBL) from 21 HCV infected patients and 14 patients with IBD, respectively, were incubated wi th Naloxone and Naloxone + Ca2+ in order to evaluate a putative modulation of PBL-mediated antibacterial activity. In fact, previous studies have demo nstrated a reduction of this T-cell activity in HCV and IBD patients. In general terms, the above treatment led to a recovery of the depressed an tibacterial activity. In some cases, increase in T lymphocyte function was obtained with Naloxone alone, while in other cases the combination Naloxone -e Ca2+ gave rise to a restorative effect. Of note, in some instances, lym phocytes were unresponsive to pharmacological modulation. The overall results suggest that beta -endorphins may down modulate T-cell antibacterial response in HCV and in IBD patients by saturating peripheral receptors on immune cells. Therefore, it is likely that Naloxone and/or Nal ox-one + Ca2+ may displace opioid drugs, thus antagonizing their effects.