Differential alteration of functions of rat peritoneal macrophages responsive to endogenous opioid peptide endomorphin-1.
Endomorphin-1 is a recently isolated endogenous opioid peptide, and potent and selective high affinity mu-opioid receptor agonist. We evaluate the role of endomorphin-1 on macrophage functions. Endomorphin-1 potentiated macrophage adhesion and the expression of adhesion molecule Mac-1 on macrophages. However, endomorphin-1 did not alter phagocytosis of Escherichia coli by macrophages. Moreover, endomorphin-1 inhibited macrophage chemotaxis and the production of superoxide anion by macrophages. On the contrary, endomorphin-1 inhibited TNF-alpha production by macrophages stimulated with both LPS and PMA, respectively. Similarly, endomorphin-1 suppressed IL-10 and IL-12 productions in response to LPS. In contrast, endomorphin-1 potentiated IL-1beta production by macrophages stimulated with PMA. These results suggest that endomorphin-1 may alter macrophage functions such as cytokine productions and functions related to natural host defense.[1]References
- Differential alteration of functions of rat peritoneal macrophages responsive to endogenous opioid peptide endomorphin-1. Inui, Y., Azuma, Y., Ohura, K. Int. Immunopharmacol. (2002) [Pubmed]
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