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Modulation of lipopolysaccharide-induced production of cytokines by methionine-enkephalin
Abstract:
In the present study, we have examined the effect of opioid peptide methionine enkephalin (MENK) on production of factors with interleukin-1 (IL-1) and tumor necrosis factor (TNF) activity by mouse peritoneal macrophages and assessed whether modification in the production of those cytokines could be related to alteration of phagocytosis by MENK. None of the MENK concentrations examined altered IL-1 or TNF activity alone. However, peritoneal macrophages co-stimulated with 1 microgram of lipopolysaccharide (LPS) and 10(-10) M MENK potentiated IL-1 activity, compared to LPS alone, but abrogated TNF activity induced by LPS. While MENK alone slightly decreased phagocytosis of sheep red blood cells (SRBC) by mouse peritoneal macrophages, cells simultaneously incubated with 1 microgram of LPS and 10(-10) M MENK had increased phagocytosis compared to LPS alone. Moreover, phagocytosis of SRBC by cells incubated overnight with the supernatant of the respective cell culture was significantly augmented. These results provide additional evidence for the immunoregulatory role of neuropeptides and suggest that the modulatory action of MENK could be mediated, at least in part, through the up-regulation of cytokines, most probably IL-1 and TNF.
Insights
Methionine enkephalin (MENK) influences immune responses. MENK potentiated interleukin-1 (IL-1) and modulated tumor necrosis factor (TNF) activity, enhancing macrophage phagocytosis.
Area of Science:
- Immunology
- Neuroscience
- Cell Biology
Background:
- Opioid peptides, like methionine enkephalin (MENK), are known to interact with immune cells.
- Macrophages play a crucial role in innate and adaptive immunity, producing key cytokines such as IL-1 and TNF.
- Understanding neuropeptide modulation of immune cell function is vital for exploring novel therapeutic strategies.
Purpose of the Study:
- To investigate the effect of methionine enkephalin (MENK) on the production of interleukin-1 (IL-1) and tumor necrosis factor (TNF) by mouse peritoneal macrophages.
- To determine if MENK-induced alterations in cytokine production correlate with changes in macrophage phagocytic activity.
Main Methods:
- Mouse peritoneal macrophages were treated with varying concentrations of MENK, lipopolysaccharide (LPS), or a combination.
- Interleukin-1 (IL-1) and tumor necrosis factor (TNF) activities were measured.
- Phagocytosis of sheep red blood cells (SRBC) by macrophages was assessed.
- The effect of macrophage supernatant on SRBC phagocytosis was evaluated.
Main Results:
- MENK alone did not alter IL-1 or TNF activity.
- Co-stimulation with LPS and MENK (10(-10) M) potentiated IL-1 activity but abrogated LPS-induced TNF activity.
- MENK alone slightly decreased phagocytosis of SRBC.
- Simultaneous incubation with LPS and MENK enhanced SRBC phagocytosis compared to LPS alone.
- Overnight incubation with macrophage supernatant significantly augmented SRBC phagocytosis.
Conclusions:
- Methionine enkephalin (MENK) modulates immune cell function, demonstrating an immunoregulatory role for neuropeptides.
- MENK's modulatory effects on macrophages appear to be mediated, at least partly, through the up-regulation of cytokines, particularly IL-1 and TNF.
- These findings suggest potential therapeutic applications of MENK in modulating immune responses.