Synergic effects of mycoplasmal lipopeptides and extracellular ATP on activation of macrophages.
Mycoplasmal lipopeptides S-(2,3-bispalmitoyloxypropyl)-CGDPKHSPKSF and S-(2,3-bispalmitoyloxypropyl)-CGNNDESNISFKEK activated a monocytic cell line, THP-1 cells, to produce tumor necrosis factor alpha. The activity of the lipopeptides was augmented by ATP in a dose-dependent manner. In addition, the level of expression of mRNAs for tumor necrosis factor alpha and interleukin-1 beta, -6, and -8 was also upregulated by the lipopeptides and/or extracellular ATP, but that of interleukin-10 was not. The P2X purinergic receptor antagonists pyridoxal phosphate 6-azophenyl 2',4'-disulfonic acid and periodate-oxidized ATP suppressed the activity of ATP to augment the activation of THP-1 cells by the lipopeptides, suggesting that P2X receptors play important roles in the activity of ATP. The nuclear factor kappa B inhibitor dexamethasone also suppressed the activity, suggesting that the activity of ATP is dependent upon the nuclear factor kappa B. Thus, these results suggest that the interaction of extracellular ATP with the P2X receptors is attributed to the activity of ATP to augment the activation of THP-1 cells by mycoplasmal lipopeptides.
Into
Takeshi
T
Department of Oral Pathobiological Science, Hokkaido University Graduate School of Dental Medicine, Kita-ku, Sapporo 060-8586, Japan.
Fujita
Mari
M
Okusawa
Tsugumi
T
Hasebe
Akira
A
Morita
Manabu
M
Shibata
Ken-Ichiro
K
D000255:Adenosine Triphosphate / Q000378:metabolism / Q000494:pharmacology*; D001425:Bacterial Outer Membrane Proteins / Q000737:chemistry / Q000494:pharmacology*; D001426:Bacterial Proteins / Q000737:chemistry / Q000494:pharmacology*; D002460:Cell Line; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D003907:Dexamethasone / Q000494:pharmacology; D004075:Diglycerides / Q000737:chemistry / Q000494:pharmacology*; D029721:Drosophila Proteins; D004357:Drug Synergism; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D055666:Lipopeptides; D008074:Lipoproteins / Q000737:chemistry / Q000494:pharmacology*; D008262:Macrophage Activation; D008562:Membrane Glycoproteins / Q000235:genetics; D015394:Molecular Structure; D009000:Monocytes / Q000166:cytology / Q000187:drug effects; D009842:Oligopeptides / Q000737:chemistry / Q000494:pharmacology*; D058919:Purinergic P2 Receptor Antagonists; D012333:RNA, Messenger; D011956:Receptors, Cell Surface / Q000235:genetics; D018048:Receptors, Purinergic P2 / Q000235:genetics; D051216:Toll-Like Receptor 6; D051193:Toll-Like Receptors; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D001425:Bacterial Outer Membrane Proteins; D001426:Bacterial Proteins; D016207:Cytokines; D004075:Diglycerides; D029721:Drosophila Proteins; C460864:FSL-1 lipoprotein, synthetic; D055666:Lipopeptides; D008074:Lipoproteins; C417669:Lp44 lipopeptide; D008562:Membrane Glycoproteins; D009842:Oligopeptides; D058919:Purinergic P2 Receptor Antagonists; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D018048:Receptors, Purinergic P2; C495368:TLR6 protein, human; D051216:Toll-Like Receptor 6; D051193:Toll-Like Receptors; D014409:Tumor Necrosis Factor-alpha; D003907:Dexamethasone; D000255:Adenosine Triphosphate; C106335:macrophage stimulatory lipopeptide 2