Inhibitory effect of N-palmitoylphosphatidylethanolamine on macrophage phagocytosis through inhibition of Rac1 and Cdc42.
The production of N-acylethanolamine (NAE) is enhanced during inflammation. NAE is synthesized from phosphatidylethanolamine with N-acylphosphatidylethanolamine (NAPE) as a precursor. The amount of NAPE at the site of inflammation exceeds that of NAE. This evokes the possibility that NAPE possesses a biological function, as does NAE. We here examined if N-palmitoylphosphatidylethanolamine (NPPE), a precursor of N-palmitoylethanolamine, modulates the state of inflammation. We found that the level of the phagocytosis of latex beads, Staphylococcus aureus, Escherichia coli, or apoptotic cells by mouse peritoneal macrophages or J774A.1 macrophages was reduced in the presence of liposomes containing NPPE, while that of dextran remained unaffected. This action of NPPE seemed to be due to the inhibition of the activation of Rac1 and Cdc42 in macrophages. These results suggested that NAPE is bioactive lipid acting toward the termination of inflammation.
Shiratsuchi
Akiko
A
Graduate School of Natural Science and Technology; Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa, Japan.
Ichiki
Manami
M
Okamoto
Yasuo
Y
Ueda
Natsuo
N
Sugimoto
Naotoshi
N
Takuwa
Yoh
Y
Nakanishi
Yoshinobu
Y
D000818:Animals; D002448:Cell Adhesion; D002478:Cells, Cultured; D005260:Female; D008081:Liposomes / Q000737:chemistry; D008246:Lysophospholipids / Q000494:pharmacology*; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism*; D051379:Mice; D008815:Mice, Inbred Strains; D010587:Phagocytosis; D020764:cdc42 GTP-Binding Protein / Q000037:antagonists & inhibitors* / Q000378:metabolism; D020830:rac1 GTP-Binding Protein / Q000037:antagonists & inhibitors* / Q000378:metabolism
D008081:Liposomes; D008246:Lysophospholipids; C067565:1-palmitoylphosphatidylethanolamine; D020764:cdc42 GTP-Binding Protein; D020830:rac1 GTP-Binding Protein