Effects of Sho-Saiko-To on Production of Prostaglandin E2 (PGE2), Leukotriene B4 (LTB4) and Superoxide from Peripheral Monocytes and Polymorphonuclear Cells Isolated from HIV Infected Individuals

1996 ◽  
Vol 24 (01) ◽  
pp. 1-10 ◽  
Author(s):  
Koji Miyamoto ◽  
Michael Lange ◽  
George McKinley ◽  
Christine Stavropoulos ◽  
Shin-ichi Moriya ◽  
...  
Keyword(s):  
Chinese Medicine ◽  
Immune Reaction ◽  
Calcium Ionophore ◽  
Leukotriene B4 ◽  
Calcium Ionophore A23187 ◽  
The Other ◽  
Control Group ◽  
Ionophore A23187 ◽  
Polymorphonuclear Cells ◽  
Healthy Control

The effects of Sho-saiko-to (SST), a traditional Chinese medicine, on the production of PGE2 from monocytes, LTB4 and superoxide from polymorphonuclear cells (PMNC) in HIY infected individuals were studied. SST inhibited the production of PGE2 from monocytes stimulated by opsonized zymosan in all groups including the healthy control group and also inhibited the production of superoxide from PMNC after stimulation with FMLP. On the other hand, SST enhanced the production of LTB4 when PMNC were stimulated by the calcium ionophore A23187. These results suggest that SST has different effects on the production of prostanoids or superoxide from monocytes and PMNC. Furthermore, our data indicates that inhibition of PGE2 or superoxide production will lead to indirect suppression of HIV, and enhancement of LTB4 will contribute to the upregulation of the immune reaction in my infected individuals.

scholarly journals Platelet-activating factor both stimulates and "primes" human polymorphonuclear leukocyte actin filament assembly

Blood ◽  
1987 ◽  
Vol 70 (6) ◽  
pp. 1921-1927 ◽  
Author(s):  
M Shalit ◽  
GA Dabiri ◽  
FS Southwick
Keyword(s):  
Actin Filament ◽  
Polymorphonuclear Leukocyte ◽  
Actin Polymerization ◽  
Platelet Activating Factor ◽  
Calcium Ionophore ◽  
Leukotriene B4 ◽  
Calcium Ionophore A23187 ◽  
Optimal Concentration ◽  
Ionophore A23187 ◽  
Filament Assembly

Abstract The phospholipid inflammatory mediator, platelet-activating factor (PAF), can stimulate polymorphonuclear leukocyte (PMN) chemotaxis. Conversion of cytoplasmic actin from monomers to filaments is associated with PMN motile functions. Using the fluorescent actin filament stain nitrobenzodiaxole phallicidin, we have investigated PAF's effects on human PMN actin polymerization. Concentrations of PAF between 1 x 10(-11) to 1 x 10(-6) mol/L induced actin filament (F- actin) assembly. An optimal concentration of PAF (1–5 x 10(-8) mol/L) induced a significantly lower rise in relative F-actin content (1.72 +/- 0.07 SEM) than an optimal concentration (5 x 10(-7) mol/L) of the chemotactic peptide FMLP (2.21 +/- 0.06). Unlike FMLP (F-actin content: 1.25 +/- 0.04 at five seconds), PAF stimulation was associated with a delay of more than five seconds (1.04 +/- 0.01 at five seconds) before an increase in F-actin could be detected. F-actin concentration reached maximum levels by 30 to 60 seconds. Prolonged stimulation (20 minutes) with PAF was associated with two phases of polymerization and depolymerization. Like FMLP, the initiation of actin filament assembly by PAF required receptor occupancy, this reaction being totally blocked by the PAF receptor inhibitor, SKI 63–441. As evidenced by the lack of inhibition by nordihydroguaiaretic acid (5 to 20 mumol/L), the production of leukotriene B4 was not required for the PAF-induced changes in F-actin. Like FMLP, PAF's ability to stimulate PMN actin polymerization was inhibited by pertussis toxin (.05 to 2.5 micrograms/mL) but not impaired by the addition of EGTA and/or the calcium ionophore A23187. Preincubation with 1 x 10(-11) to 1 x 10(-8) mol/L PAF for 2 to 60 minutes enhanced the rise in F-actin content induced by low concentrations of FMLP (5 x 10(-12) to 1 x 10(-10) mol/L) indicating that this phospholipid was capable of “priming” the PMN actin polymerization response.

Dibutyryl Cytidine and Adenosine 3':5'-Cyclic Monophosphates Inhibit A23187-Stimulated Rat Peritoneal Macrophage Leukotriene B4 Synthesis

1988 ◽  
Vol 1 (2) ◽  
pp. 109-114
Author(s):  
G. R. Elliott ◽  
A. P. M. Lauwen ◽  
I. L. Bonta
Keyword(s):  
Peritoneal Macrophage ◽  
Calcium Ionophore ◽  
Peritoneal Macrophages ◽  
Leukotriene B4 ◽  
Calcium Ionophore A23187 ◽  
Intracellular Camp ◽  
Ionophore A23187 ◽  
Eicosanoid Release ◽  
Stable Product

Dibutyryl cytidine and adenosine 3':5'-cyclic monophosphates (db-cCMP and db-cAMP respectively) inhibited the synthesis of thromboxane (TX) B2, the stable product of TXA2, and leukotriene (LT) B4 by 4-day carrageenin-elicited rat peritoneal macrophages stimulated by the calcium ionophore A23187. Incubation of macrophages with dbcAMP, at concentrations inhibiting eicosanoid release, was associated with an increase in intracellular cAMP concentrations. No such increase was seen when db-cCMP was used.

scholarly journals Tulathromycin Exerts Proresolving Effects in Bovine Neutrophils by Inhibiting Phospholipases and Altering Leukotriene B4, Prostaglandin E2, and Lipoxin A4Production

2014 ◽  
Vol 58 (8) ◽  
pp. 4298-4307 ◽  
Author(s):  
Carrie D. Fischer ◽  
Stephanie C. Duquette ◽  
Bernard S. Renaux ◽  
Troy D. Feener ◽  
Douglas W. Morck ◽  
...  
Keyword(s):  
Calcium Ionophore ◽  
Leukotriene B4 ◽  
Calcium Ionophore A23187 ◽  
Lipid Signaling ◽  
Prostaglandin E ◽  
Ionophore A23187 ◽  
Proinflammatory Mediators ◽  
Bovine Neutrophils

ABSTRACTThe accumulation of neutrophils and proinflammatory mediators, such as leukotriene B4(LTB4), is a classic marker of inflammatory disease. The clearance of apoptotic neutrophils, inhibition of proinflammatory signaling, and production of proresolving lipids (including lipoxins, such as lipoxin A4[LXA4]) are imperative for resolving inflammation. Tulathromycin (TUL), a macrolide used to treat bovine respiratory disease, confers immunomodulatory benefits via mechanisms that remain unclear. We recently reported the anti-inflammatory properties of TUL in bovine phagocytesin vitroand inMannheimia haemolytica-challenged calves. The findings demonstrated that this system offers a powerful model for investigating novel mechanisms of pharmacological immunomodulation. In the present study, we examined the effects of TUL in a nonbacterial model of pulmonary inflammationin vivoand characterized its effects on lipid signaling. In bronchoalveolar lavage (BAL) fluid samples from calves challenged with zymosan particles (50 mg), treatment with TUL (2.5 mg/kg of body weight) significantly reduced pulmonary levels of LTB4and prostaglandin E2(PGE2). In calcium ionophore (A23187)-stimulated bovine neutrophils, TUL inhibited phospholipase D (PLD), cytosolic phospholipase A2(PLA2) activity, and the release of LTB4. In contrast, TUL promoted the secretion of LXA4in resting and A23187-stimulated neutrophils, while levels of its precursor, 15(S)-hydroxyeicosatetraenoic acid [15(S)-HETE], were significantly lower. These findings indicate that TUL directly modulates lipid signaling by inhibiting the production of proinflammatory eicosanoids and promoting the production of proresolving lipoxins.

scholarly journals Is a rise in intracellular concentration of free calcium necessary or sufficient for stimulated cytoskeletal-associated actin?

1986 ◽  
Vol 102 (4) ◽  
pp. 1459-1463 ◽  
Author(s):  
R I Sha'afi ◽  
J Shefcyk ◽  
R Yassin ◽  
T F Molski ◽  
M Volpi ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Pertussis Toxin ◽  
Incubation Medium ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Extracellular Calcium ◽  
Intracellular Concentration ◽  
The Other ◽  
Free Calcium ◽  
Ionophore A23187

The addition of the calcium ionophore A23187 to rabbit neutrophils increases the amount of actin associated with the cytoskeleton regardless of the presence or absence of calcium in the incubation medium. In the presence of extracellular calcium, the effect of A23187 is biphasic with respect to concentration. The action of the ionophore is rapid, transient, and is inhibited by pertussis toxin, hyperosmolarity, and quinacrine. On the other hand, the addition of pertussis toxin or hyperosmolarity has small if any, effect on the rise in intracellular calcium produced by A23187. While quinacrine does not affect the fMet-Leu-Phe-induced increase in cytoskeletal actin and the polyphosphoinositide turnover, its addition inhibits completely the stimulated increase in Ca-influx produced by the same stimulus. The results presented here suggest that a rise in the intracellular concentration of free calcium is neither necessary nor sufficient for the stimulated increase in cytoskeletal-associated actin. A possible relationship between the lipid remodeling stimulated by chemoattractants and the increased cytoskeletal actin is discussed.

scholarly journals The inhibition of neutrophil granule enzyme secretion and chemotaxis by pertussis toxin.

1985 ◽  
Vol 100 (5) ◽  
pp. 1641-1646 ◽  
Author(s):  
E L Becker ◽  
J C Kermode ◽  
P H Naccache ◽  
R Yassin ◽  
M L Marsh ◽  
...  
Keyword(s):  
Pertussis Toxin ◽  
Regulatory Protein ◽  
Calcium Ionophore ◽  
Leukotriene B4 ◽  
Calcium Ionophore A23187 ◽  
Chemotactic Factor ◽  
Target Protein ◽  
Enzyme Secretion ◽  
Ionophore A23187 ◽  
Dependent Inhibition

Pertussis toxin treatment of rabbit peritoneal neutrophils causes a concentration-dependent inhibition of granule enzyme secretion induced by formylmethionyl-leucyl-phenylalanine, C5a, and leukotriene B4. It also inhibits chemotaxis induced by formylmethionyl-leucyl-phenylalanine. The same toxin treatment, however, has no effect on granule enzyme secretion induced by the calcium ionophore A23187 or phorbol 12-myristate 13-acetate. Moreover, pertussis toxin treatment does not affect either the number or affinity of the formylpeptide receptors on the neutrophil nor does it have any effect on the unstimulated levels of cyclic AMP (cAMP) or the transient rise in cAMP induced by chemotactic factor stimulation in these cells. We hypothesize that pertussis toxin, as in other cells, interacts with a GTP binding regulatory protein identical with or analogous to either Ni or transducin which mediates the receptor-induced inhibition or activation of a target protein or proteins required in neutrophil activation. The nature of the target protein is unknown, but it is not the catalytic unit of adenylate cyclase. The target protein acts after binding of chemotactic factor to its receptor in the sequence that leads to the receptor-induced rise in intracellular Ca2+. It does not affect the responses elicited by the direct introduction of calcium into the cells or the activity of protein kinase C.

Inhibitory effects of calcium ionophore pretreatment of porcine oocytes on polyspermic fertilization

Zygote ◽  
2006 ◽  
Vol 14 (1) ◽  
pp. 17-22 ◽  
Author(s):  
T. Hayashi ◽  
H. Sato ◽  
H. Iwata ◽  
T. Kuwayama ◽  
Y. Monji
Keyword(s):  
Calcium Ionophore ◽  
Inhibitory Effect ◽  
Calcium Ionophore A23187 ◽  
The Other ◽  
Ionophore A23187 ◽  
Inhibitory Effects ◽  
High Concentration ◽  
Maturation Period ◽  
Low Concentration ◽  
Other Hand

The present study examined the inhibitory effects of various pretreatment concentrations (0–100 μM) of the calcium ionophore A23187 on polyspermic fertilization and then examined the effect of the maturation period and the time between calcium ionophore treatment and fertilization on the inhibitory effect of calcium ionophore on polyspermic fertilization. In experiment 1, a high concentration of calcium ionophore (100 μM) increased the rate of activated oocytes, but the rate of fertilization declined. On the other hand, when oocytes were treated with a low concentration of calcium ionophore (10 μM), monospermic fertilization was significantly increased (10 μM; 31.3%) (p < 0.05). In experiment 2, oocytes were cultured for various times (0, 0.5, 3, 6 h) after calcium ionophore treatment (10 μM) before fertilization. The highest rate of monospermic fertilization was detected in the oocytes cultured for 6 h after calcium ionophore treatment before fertilization. In experiments 3 and 4, we examined the effect of the maturation period (40 h or 44 h) on the rate of fertilization and blastulation of oocytes pretreated with calcium ionophore. The treatment of oocytes with calcium ionophore significantly decreased the rate of polyspermic fertilization regardless of the maturation period (44 h: with calcium ionophore 26.25% vs without 78.8%; 40 h: with calcium ionophore 37.5% vs without 77.5%); however, calcium ionophore treatment increased the rates of monospermic fertilization and blastulation of the oocytes matured for 44 h, but not those matured for 40 h. In conclusion, activation with a low concentration of calcium ionophore (10 μM) and a further 6 h of culture before fertilization improved the rate of monospermic fertilization and blastulation.

Potentiation of pepsinogen secretion from dispersed glands from rat stomach

1983 ◽  
Vol 245 (4) ◽  
pp. G525-G530 ◽  
Author(s):  
J. P. Raufman ◽  
D. K. Kasbekar ◽  
R. T. Jensen ◽  
J. D. Gardner
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Phosphodiesterase Inhibitor ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
The Other ◽  
Ionophore A23187 ◽  
Rat Stomach ◽  
Gastric Glands ◽  
Cellular Calcium ◽  
Pepsinogen Secretion

In the present study we examined the actions of various agents alone and in combination on pepsinogen secretion from dispersed gastric glands prepared from rat stomach. Potentiation of pepsinogen secretion occurred with secretin or vasoactive intestinal peptide plus carbamylcholine or cholecystokinin. The pattern of action of secretin and vasoactive intestinal peptide could be reproduced by 8-bromo-cAMP, and the pattern of action of carbamylcholine and cholecystokinin could be reproduced by the calcium ionophore A23187. A phosphodiesterase inhibitor, isobutylmethylxanthine, increased pepsinogen secretion, increased the potency but not the efficacy of the action of secretin on pepsinogen secretion, and potentiated the action of carbamylcholine on pepsinogen secretion. These results suggest that, in dispersed gastric glands from rat stomach, secretagogue-induced pepsinogen secretion can be stimulated by two different mechanisms: one mechanism is mediated by cAMP and the other is mediated by changes in cellular calcium. Secretagogues whose actions are mediated by one mechanism potentiate the actions of those secretagogues whose actions are mediated by the other mechanism.

scholarly journals Leukotriene generation by eosinophils.

1982 ◽  
Vol 155 (2) ◽  
pp. 390-402 ◽  
Author(s):  
A Jörg ◽  
W R Henderson ◽  
R C Murphy ◽  
S J Klebanoff
Keyword(s):  
Arachidonic Acid ◽  
Calcium Ionophore ◽  
Leukotriene B4 ◽  
Arachidonic Acid Metabolism ◽  
Calcium Ionophore A23187 ◽  
Eicosatetraenoic Acid ◽  
Gas Chromatography Mass Spectrometry ◽  
Ionophore A23187 ◽  
Lipoxygenase Pathway ◽  
Leukotriene D4

Horse eosinophils purified to greater than 98% generated slow reacting substance (SRS) when incubated with the calcium ionophore A23187. On a per cell basis, eosinophils generated four to five times the SRS produced by similarly treated horse neutrophils. Eosinophil SRS production was inhibited by 5,8,11,14-eicosatetraynoic acid and augmented by indomethacin and arachidonic acid, suggesting that it was a product(s) of the lipoxygenase pathway of arachidonic acid metabolism. Compounds with SRS activity were purified by high-pressure liquid chromatography (HPLC) and identified by ultraviolet spectra, spectral shift on treatment with lipoxygenase, incorporation of [14C]arachidonic acid, gas chromatography-mass spectrometry, and comparison of retention times on HPLC to authentic standards. The eosinophil products characterized were 5-(S), 12-(R)-dihydroxy-6-cis-8, 10-trans-14-cis-eicosatetraenoic acid (leukotriene B4) and its 5-(S), 12-(R)-6-trans and 5-(S), 12-(S)-6-trans isomers, 5-(S)-hydroxy-6-(R)-S-glutathionyl-7,9-trans-11, 14-cis-eicosatetraenoic acid (leukotriene C4) and its 11-trans isomer, and 5-(S)-hydroxy-6-(R)-S-cysteinylglycine-7,9-trans-11,14-cis-eicosatetraenoic acid (leukotriene D4).

A combination of calcium ionophore and puromycin effectively produces human parthenogenones with one haploid pronucleus

Zygote ◽  
2001 ◽  
Vol 9 (1) ◽  
pp. 83-88 ◽  
Author(s):  
Koji Nakagawa ◽  
Shuji Yamano ◽  
Hisayo Nakasaka ◽  
Kenji Hinokio ◽  
Midori Yoshizawa ◽  
...  
Keyword(s):  
Polar Body ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Control Group ◽  
Ionophore A23187 ◽  
Cleavage Rate ◽  
Parthenogenetic Activation ◽  
Second Polar Body ◽  
Activation Rates ◽  
Pronuclear Formation

Parthenogenetic activation with various combinations of the calcium ionophore A23187 and protein synthesis or phosphorylation inhibitors was investigated as a means of producing human parthenogenones with one haploid pronucleus. Unfertilised human aged oocytes exposed to 5 μM A23187 for 5 min were treated with 10 μg/ml puromycin (puromycin group, 46 oocytes) or 2 mM 6-dimethylaminopurine (DMAP group, 42 oocytes) for 5 h. Oocytes treated only with A23187 served as a control (control group, 40 oocytes). After washing the oocytes, they were incubated for up to 37 h. Evidence of activation (pronuclear formation) and cleavage was observed 18 h and 42 h after A23187 treatment, respectively. Activation rates in the puromycin and DMAP groups were significantly higher than in the control group (91% (42/46) and 77% (34/44) vs 20% (8/40), p < 0.05, respectively). In the puromycin group, 81% (34/42) of the activated oocytes showed one pronucleus with the second polar body (2ndPB), whereas none (0/34) of the activated oocytes in the DMAP group extruded the 2ndPB. The cleavage rate in the puromycin group was significantly lower than in the DMAP group (38% vs 68%, p < 0.05). The activated oocytes which had one pronucleus with the 2ndPB in the puromycin group showed a haploid set of chromosomes (10/13). In conclusion, the combination of A23187 and puromycin is effective for producing human parthenogenones with one haploid pronucleus.

Chronically Impaired Endothelial Vasoreactivity Following Oversized Endovascular Introducer Sheath Placement in Porcine Iliac Arteries: Implications for Endovascular Therapy

Vascular ◽  
2006 ◽  
Vol 14 (6) ◽  
pp. 353-361 ◽  
Author(s):  
Peter H. Lin ◽  
James L. Steinberg ◽  
Tamuru Okada ◽  
Wei Zhou ◽  
Hosam F. El Sayed ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Time Course ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Control Group ◽  
Ionophore A23187 ◽  
Introducer Sheath ◽  
Iliac Arteries ◽  
Endovascular Prosthesis

The conventional endovascular aortic aneurysm procedure entails the placement of oversized introducer sheaths in relatively normal ileofemoral arteries to allow the delivery and deployment of endovascular prosthesis. Endoluminal manipulation with passage of oversized endoluminal devices can lead to endothelial denudation, resulting in impaired cellular function. The purpose of this study was to assess the time course of endothelial function with vasoreactivity following oversized endovascular sheath insertion ranging from 1 day to 16 weeks in normal porcine iliac arteries. Following oversized introducer sheath placement in bilateral iliac arteries, vasoreactivity was tested using both endothelium-dependent and -independent vasodilators. Intravascular ultrasonography showed a significant reduction in the luminal area at 12 and 16 weeks. This was similarly supported by morphometric analysis, which showed increased medial thickness with an elevated intima to media ratio at the same time course. Endothelium-dependent relaxation to bradykinin, calcium ionophore A23187, serotonin, and adenosine diphosphate all uniformly displayed attenuated endothelial dysfunction at all time points when compared with the control group. In contrast, endothelium-independent relaxation showed a decreased vasoresponsiveness at 4 weeks. In conclusion, this study underscored the detrimental and chronic endothelial dysfunction in a normal artery caused by oversized introducer sheath placement. Chronically impaired endothelial function may play a role leading to iliofemoral artery thrombosis or late occlusion, which were well-recognized adverse events following endovascular aneurysm procedures. Our study underscores the importance of appropriate patient selection to minimize potential sheath oversize and endograft device miniaturization to avoid vessel wall injury and maintain vasoreactivity.

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