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Enkephalins-modulation of Plasmodium cynomolgi antigens-induced colony-stimulating factors elaboration by macrophages
P P Singh1, S Singh, V C Dhawan
1Division of Microbiology, Central Drug Research Institute, Lucknow, India.
Abstract:
Methionine-enkephalin (M-Enk) and its analogue compound 82/205 (10(-5) and 10(-6) M) inhibited elaboration of Plasmodium cynomolgi total antigens soluble in culture medium (P.c.SA)-induced colony-stimulating factors (CSFs) by monkey blood monocyte-derived macrophages, in vitro. Paradoxically, lower concentrations (10(-7)-10(-9) M) of both the peptides greatly augmented CSFs elaboration; 82/205 appeared to be nearly 2.3-fold more potent. Naloxone (10(-5) M) pretreatment of macrophages inhibited only the M-Enk- and 82/205-induced enhanced CSFs elaboration, suggesting an opiate receptors-mediated mechanism of action. None of the peptides or naloxone (10(-5)-10(-9) M) had any direct effect on the CSF elaboration by unstimulated macrophages.
Insights
Methionine-enkephalin and its analogue modulate colony-stimulating factors (CSFs) production by macrophages. Opiate receptor involvement suggests a potential therapeutic target for malaria-associated immune responses.
Area of Science:
- Immunology
- Neuroscience
- Parasitology
Background:
- Colony-stimulating factors (CSFs) are crucial for immune cell development and function.
- Opioid peptides, like methionine-enkephalin (M-Enk), can influence immune responses.
- Plasmodium cynomolgi infections can alter host immune cell behavior.
Purpose of the Study:
- To investigate the in vitro effect of M-Enk and its analogue (82/205) on CSF elaboration by macrophages stimulated with Plasmodium antigens.
- To explore the potential involvement of opiate receptors in this interaction.
Main Methods:
- Monkey blood monocyte-derived macrophages were cultured in vitro.
- Macrophages were stimulated with Plasmodium cynomolgi soluble antigens (P.c.SA).
- The effects of M-Enk, compound 82/205, and naloxone on CSF production were assessed at various concentrations.
Main Results:
- High concentrations (10(-5) and 10(-6) M) of M-Enk and 82/205 inhibited P.c.SA-induced CSF elaboration.
- Lower concentrations (10(-7)-10(-9) M) of both peptides augmented CSF elaboration, with 82/205 being more potent.
- Naloxone pretreatment blocked the enhancing effect of the peptides, indicating an opiate receptor-mediated mechanism.
Conclusions:
- M-Enk and its analogue exhibit dose-dependent effects on macrophage CSF production in response to Plasmodium antigens.
- The observed augmentation of CSFs at lower peptide concentrations is mediated through opiate receptors.
- These findings suggest a complex interplay between opioid signaling and the immune response during malaria.