The research group of professor Piomelli published an important and fundamental paper on the role of macrophages in our immunesystem and palmitoylethanolamide as a vehicle for the macrophages to combat inflammation.
They start describing macrophages as multi-faceted phagocytic effector cells that derive from circulating monocytes and undergo differentiation in target tissues to regulate key aspects of the inflammatory process.
They followup by pointing out that macrophages produce and degrade a variety of lipid mediators that stimulate or suppress pain and inflammation such as the fatty acid ethanolamides (FAEs), among which palmitoylethanolamide(PEA).
PEA, they continue, has recently emerged as important intrinsic regulators of nociception and inflammation.
PEA is released from the membrane precursor, N-acylphosphatidylethanolamine (NAPE), and in macrophage are primarily deactivated by the lysosomal cysteine amidase, N-acylethanolamine acid amidase (NAAA). Via PEA the macrophages can exerte a tight control over the ability of these lipid mediators to activate the nuclear power-switch to switch off overactive inflammation, the PPAR-α and thus attenuate the inflammatory response.
PEA therefore can be seen as an important and biological tool to treat chronic inflammatory disorders.
From earlier studies we already gathered that palmitoylethanolamide stimulates phagocytosis of bacteria by macrophages and thus can increases the resistance of mice against infections!
Pontis S, Ribeiro A, Sasso O, Piomelli D. Macrophage-derived lipid agonists of PPAR-α as intrinsic controllers of inflammation. Crit Rev Biochem Mol Biol. 2015 Nov 20:1-8.
Sandra Redlich, Sandra Ribes, Sandra Schütze and Roland Nau Palmitoylethanolamide stimulates phagocytosis of Escherichia coli K1 by macrophages and increases the resistance of mice against infections. Journal of Neuroinflammation 2014, 11:108 doi:10.1186/1742-2094-11-108