Activation of Peritoneal Macrophages by Platelet-Activating Factor (Paf) and Glyceroglycolipid

2015 ◽  
pp. 163-168
Author(s):  
Keizo Inoue ◽  
Ichiro Kudo ◽  
Hidetoshi Hayashi ◽  
Mikihiko Naito ◽  
Hiroaki Nomura ◽  
...  
Keyword(s):  
Platelet Activating Factor ◽  
Peritoneal Macrophages

scholarly journals Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages

1992 ◽  
Vol 1 (6) ◽  
pp. 375-377 ◽  
Author(s):  
Fang Jun ◽  
Zheng Qin Yue ◽  
Wang Hong Bin ◽  
Ju Dian Wen ◽  
Yi Yang Hua
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Inflammatory Mediator ◽  
Platelet Activating Factor ◽  
Peritoneal Macrophages ◽  
Dependent Manner ◽  
Anti Inflammatory ◽  
Dose Dependent ◽  
Necrosis Factor ◽  
Inflammatory Effect

Esculentoside A (EsA) is a saponin isolated from the roots of Phytolacca esculenta. Previous experiments showed that it had strong anti-inflammatory effects. Tumour necrosis factor (TNF) is an important inflammatory mediator. In order to study the mechanism of the anti-inflammatory effect of EsA, it was determined whether TNF production from macrophages was altered by EsA under lipopolysaccharide (LPS) stimulated conditions. EsA was found to decrease both extracellular and cell associated TNF production in a dose dependent manner at concentrations higher than 1 μmol/l EsA. Previous studies have showed that EsA reduced the releasing of platelet activating factor (PAF) from rat macrophages. The reducing effects of EsA on the release of TNF and PAF may explain its anti-inflammatory effect.

scholarly journals A murine platelet-activating factor receptor gene: cloning, chromosomal localization and up-regulation of expression by lipopolysaccharide in peritoneal resident macrophages

1996 ◽  
Vol 314 (2) ◽  
pp. 671-678 ◽  
Author(s):  
Satoshi ISHII ◽  
Yoichi MATSUDA ◽  
Motonao NAKAMURA ◽  
Iwao WAGA ◽  
Kazuhiko KUME ◽  
...  
Keyword(s):  
Lipid A ◽  
Receptor Gene ◽  
Platelet Activating Factor ◽  
Peritoneal Macrophages ◽  
Regulation Of Expression ◽  
Gene Encoding ◽  
Platelet Activating Factor Receptor ◽  
Factor Α ◽  
Necrosis Factor

A murine gene encoding a platelet-activating factor receptor (PAFR) was cloned. The gene was mapped to a region of the D2.2 band of chromosome 4 both by fluorescence in situ hybridization and by molecular linkage analysis. Northern blot analysis showed a high expression of the PAFR message in peritoneal macrophages. When C3H/HeN macrophages were treated with bacterial lipopolysaccharide (LPS) or synthetic lipid A, the PAFR gene expression was induced. Bacterial LPS, but not lipid A, induced the level of PAFR mRNA in LPS-unresponsive C3H/HeJ macrophages. These induction patterns were parallel to those of tumour necrosis factor-α mRNA. Thus the PAFR in macrophages is important in LPS-induced pathologies.

scholarly journals Tumor necrosis factor/cachectin stimulates peritoneal macrophages, polymorphonuclear neutrophils, and vascular endothelial cells to synthesize and release platelet-activating factor.

1987 ◽  
Vol 166 (5) ◽  
pp. 1390-1404 ◽  
Author(s):  
G Camussi ◽  
F Bussolino ◽  
G Salvidio ◽  
C Baglioni
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Vascular Endothelial Cells ◽  
Platelet Activating Factor ◽  
Peritoneal Macrophages ◽  
Dermal Fibroblasts ◽  
Polymorphonuclear Neutrophils ◽  
Vascular Endothelial ◽  
Necrosis Factor

Murine tumor necrosis factor (mTNF) stimulates production of platelet-activating factor (PAF) by cultured rat peritoneal macrophages in amounts comparable to those formed during treatment with the calcium ionophore A23187 or phagocytosis of zymosan. The cell-associated PAF that was released into the medium was identical to synthetic PAF, as determined with physicochemical, chromatographic, and enzymatic assays. Furthermore, de novo synthesis of PAF by macrophages was demonstrated by the incorporation of radioactive precursors such as [3H]acetyl-coenzyme A or [3H]2-lyso-PAF. Macrophages incubated with mTNF for 4 h synthesized PAF only during the first h of treatment. At this time, the amount of cell-associated PAF was approximately equal to that released into the medium. The cell-associated PAF decreased afterwards, whereas that in the medium did not correspondingly increase, suggesting that some PAF was being degraded. The response of rat macrophages to different doses of mTNF and human TNF (hTNF) was examined. Maximal synthesis of PAF was obtained with 10 ng/ml of mTNF and 50 ng/ml of hTNF. This finding may be explained by a lower affinity of hTNF for TNF receptors of rat cells. The hTNF stimulated production of PAF by human vascular endothelial cells cultured from the umbilical cord vein. The time course of PAF synthesis was slower than that observed with macrophages, with maximal production between 4 and 6 h of treatment. Optimal synthesis of PAF was obtained with 10 ng/ml of hTNF. Only 20-30% of the PAF synthesized by endothelial cells was released into the medium, even after several hours of incubation. Synthesis of PAF in response to TNF was also detected in rat polymorphonuclear neutrophils, but not in human tumor cells and dermal fibroblasts. Therefore, production of PAF is a specialized response that is transient in macrophages continuously treated with TNF, and that appears to be controlled by unidentified regulatory mechanisms.

Possible participation of intracellular platelet-activating factor in NF-κB activation in rat peritoneal macrophages

2002 ◽  
Vol 1583 (1) ◽  
pp. 26-34 ◽  
Author(s):  
Kousei Tsuyuki ◽  
Gaku Ichinowatari ◽  
Atsuo Tanimoto ◽  
Masateru Yamada ◽  
Hiroshi Yaginuma ◽  
...  
Keyword(s):  
Platelet Activating Factor ◽  
Peritoneal Macrophages

scholarly journals Essential Role of Platelet-Activating Factor in Control of Leishmania (Leishmania)amazonensis Infection

2000 ◽  
Vol 68 (11) ◽  
pp. 6355-6361 ◽  
Author(s):  
Maria Valdrinez Campana Lonardoni ◽  
Momtchillo Russo ◽  
Sonia Jancar
Keyword(s):  
Lymph Nodes ◽  
Platelet Activating Factor ◽  
Parasite Load ◽  
Peritoneal Macrophages ◽  
Leishmania Infection ◽  
Prostaglandin E ◽  
No Production ◽  
Regional Lymph Nodes

ABSTRACT In the present study we investigated the role of platelet-activating factor (PAF) and prostaglandins in experimental Leishmania (Leishmania)amazonensis infection and the relationship between these mediators and nitric oxide (NO) production. Mouse peritoneal macrophages elicited with thioglicolate were infected with leishmania amastigotes, and the infection index determined 48 h later. The course of infection was monitored for 5 weeks in mice infected in the footpad with promastigotes by measuring the footpad swelling and parasite load in regional lymph nodes and spleen. The addition of PAF to C57BL/6 mouse macrophages significantly inhibited parasite growth and induced NO production. Treatment of macrophages with a selective PAF antagonist, WEB2086, increased the infection, indicating that endogenously produced PAF regulates macrophage ability to control leishmania infection. This effect of PAF was abolished by addition of the inhibitor of NO synthesis, L-NAME, to the cultures. The addition of prostaglandin E2 significantly increased the infection and NO production. Treatment with cyclo-oxygenase inhibitor, indomethacin, reduced the infection and PAF-induced release of NO. Thus, the increased NO production induced by PAF seems to be mediated by prostaglandins. The more-selective inhibitors of cyclo-oxygenase 2, nimesulide and NS-398, had no significant effect. Thus, antileishmanial activity correlates better with the presence of PAF or absence of prostaglandins than with NO production. In vivo treatment with PAF antagonists significantly increased leishmania lesions, as well as the parasite load, in regional lymph nodes and spleens. These findings indicate that PAF is essential for the control of leishmania infection.

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