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Leu-enkephalin enhances interferon secretion in mice
J Gabrilovac1, M Ikic-Sutlic, N Knezevic
1Rudjer Boskovic Institute, Department of Experimental Biology and Medicine, Zagreb, Croatia.
Research in Experimental Medicine. Zeitschrift Fur Die Gesamte Experimentelle Medizin Einschliesslich Experimenteller Chirurgie
|January 1, 1996
Summary
The opioid peptide leu-enkephalin (LENK) influences natural killer (NK) cell activity by altering interferon (IFN) secretion. LENK increases basal IFN levels, impacting NK activity differently over time.
Area of Science:
- Immunology
- Neuroendocrinology
Background:
- Opioid peptides modulate immune responses.
- Interferon (IFN) is a key regulator of natural killer (NK) cell activity.
Purpose of the Study:
- To investigate the relationship between leu-enkephalin (LENK)-induced alterations in NK activity and changes in IFN secretion.
- To explore the role of IFN in mediating the immunomodulatory effects of LENK.
Main Methods:
- Mice were injected with leu-enkephalin (LENK) or polyinosinic-polycytidylic acid (poly-IC).
- Splenic NK activity and plasma IFN levels were measured at 24 and 48 hours post-injection.
- Naloxone, an opioid receptor antagonist, was used to assess the involvement of opioid receptors.
Main Results:
- LENK significantly increased basal IFN secretion, comparable to poly-IC.
- LENK did not augment poly-IC-induced IFN levels.
- A delayed increase in NK activity at 48 hours post-LENK coincided with elevated IFN, while a decrease in NK activity was observed at 24 hours.
- Naloxone partially blocked LENK-induced IFN secretion and increased IFN levels independently.
Conclusions:
- The immunomodulatory effects of LENK in vivo are linked to alterations in IFN secretion.
- LENK's impact on NK activity is complex and time-dependent, involving IFN modulation.
- Opioid receptors play a partial role in LENK-induced IFN secretion.