Induction of Suppressor T Cells in Vitro by Arachidonic Acid Metabolites Issued from the Lipoxygenase Pathway

1985 ◽  
pp. 565-575 ◽  
Author(s):  
Norbert Gualde ◽  
James S. Goodwin
Keyword(s):  
T Cells ◽  
Arachidonic Acid ◽  
Suppressor T Cells ◽  
Lipoxygenase Pathway ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites

Arachidonic acid metabolites issued from the lipoxygenase pathway and lymphocyte response in vitro

1982 ◽  
Vol 4 (4) ◽  
pp. 353
Author(s):  
N. Gualde ◽  
H. Rabinovitch-Chable ◽  
M. Rigaud ◽  
M. Fredon ◽  
J. Durand ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Lymphocyte Response ◽  
Lipoxygenase Pathway ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites

Arachidonic acid metabolites induced β-adrenoceptor densitization in rat lung in vitro

1985 ◽  
Vol 30 (5) ◽  
pp. 799-809 ◽  
Author(s):  
Luisa Daffonchio ◽  
Maria Pia Abbracchio ◽  
Alicia Hernandez ◽  
Emanuela Giani ◽  
Flaminio Cattabeni ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Rat Lung ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites

Control of gap junction formation in canine trachea by arachidonic acid metabolites

1986 ◽  
Vol 250 (3) ◽  
pp. C495-C505 ◽  
Author(s):  
R. Agrawal ◽  
E. E. Daniel
Keyword(s):  
Arachidonic Acid ◽  
Gap Junctions ◽  
Gap Junction ◽  
Direct Effects ◽  
Leukotriene C4 ◽  
Lipoxygenase Pathway ◽  
Junction Formation ◽  
Acid Metabolites ◽  
Pg E2

This study examined whether the synthesis of the metabolites of arachidonic acid (AA) was involved in gap junction formation by 4-aminopyridine (4-AP) treatment in vitro in canine trachealis. Studies were made of the effects on gap junction formation of putative inhibitors of the cyclooxygenase and of both this and the lipoxygenase pathway of AA metabolism and the direct effects of prostaglandins (PG) E2 and I2. The number of gap junctions of similar size was increased after brief exposure to 4-AP. After indomethacin (IDM), 4-AP treatment decreased the number of gap junctions but did not affect their size. Pretreatment with 5,8,11,14-eicosatetraynoic acid or nordihydroguiaretic acid, putative inhibitors of cyclooxygenase and lipoxygenase enzymes, inhibited both the 4-AP-induced increase and decrease in the number of gap junctions. FPL 55712, a putative antagonist of leukotriene C4, did not alter either the number or the size of gap junctions when added alone or in combination with IDM. AA alone increased the number of gap junctions, but after IDM, AA decreased the number of gap junctions compared with the controls. Incubation of trachealis strips in vitro for 30 min with PGE2 increased the number of gap junctions by about threefold along with an increase in the size of the gap junctions. Similar incubation with PGI2, however, increased the number of gap junctions by approximately 60% without any change in the size. In the course of some control experiments, an interaction between carbachol and alcohol was observed such that alcohol caused an IDM-sensitive relaxation of carbachol-induced contractions, which was not observed when serotonin was the contractile agent. These results strongly suggest that PGE2 and PGI2 increase the formation of gap junctions in canine trachealis and that these prostanoids are released by 4-AP treatment. Leukotrienes may also be inhibitory in the formation of gap junctions, but FPL 55712 did not affect either the increase or the decrease in gap junctions after 4-AP.

Role of Arachidonic Acid Metabolites in Intracellular Enzyme Efflux from Damaged Skeletal Muscle ‘in vitro’

1986 ◽  
Vol 71 (s15) ◽  
pp. 23P-23P
Author(s):  
M.J. Jackson ◽  
A.J.M. Wagenmakers ◽  
R.H.T. Edwards
Keyword(s):  
Skeletal Muscle ◽  
Arachidonic Acid ◽  
Intracellular Enzyme ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites

The role of novel arachidonic acid metabolites in GnRH action on gonadotrophin release in vitro

1986 ◽  
Vol 1 (6) ◽  
pp. 349-352 ◽  
Author(s):  
L. Kiesel ◽  
A. Przylipiak ◽  
T. Rabe ◽  
B. Runnebaum
Keyword(s):  
Arachidonic Acid ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites ◽  
Release In Vitro

Molecular mechanism of nucleotide-induced primary granule release in human neutrophils: role for the P2Y2receptor

2004 ◽  
Vol 286 (2) ◽  
pp. C264-C271 ◽  
Author(s):  
John Meshki ◽  
Florin Tuluc ◽  
Ovidiu Bredetean ◽  
Zhongren Ding ◽  
Satya P. Kunapuli
Keyword(s):  
Arachidonic Acid ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
Extracellular Nucleotides ◽  
Human Neutrophils ◽  
Lipoxygenase Pathway ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites ◽  
Primary Granule ◽  
Granule Release

Nucleotides are released during vascular injury from activated platelets and broken cells, which could stimulate human neutrophils. In this study, we characterized the P2Y receptors and investigated the functional effects of extracellular nucleotides on human neutrophils. Pharmacological characterization using selective agonists and pertussis toxin revealed that human neutrophils express only functional P2Y2receptors. However, P2Y2receptor agonists ATP or uridine triphosphate (UTP) caused intracellular Ca2+increases in isolated human neutrophils with an EC50of 1 μM but failed to cause release of primary granules from human neutrophils. ATP and UTP were equally potent in causing elastase release from human neutrophils in the presence of exogenous soluble fibrinogen, whereas ADP and UDP were without effect. We investigated whether nucleotides depend on generated arachidonic acid metabolites to cause degranulation. However, phenidone and MK-886, inhibitors of the 5-lipoxygenase pathway, failed to block nucleotide-induced intracellular calcium mobilization and elastase release. ATP and UTP caused activation of p38 MAPK and ERK1/2 in human neutrophils. In addition, the inhibitors of the MAPK pathway, SB-203580 and U-0126, inhibited nucleotide-induced elastase release. We conclude that fibrinogen is required for nucleotide-induced primary granule release from human neutrophils through the P2Y2receptor without a role for arachidonic acid metabolites. Both ERK1/2 and p38 MAPK play an important role in nucleotide-induced primary granule release from human neutrophils.

Effect of Lipoxygenase Inhibition on Mucous Glycoprotein Secretion from Chinchilla Middle Ear Fpithelial Cells in Vitro

1996 ◽  
Vol 105 (11) ◽  
pp. 916-921 ◽  
Author(s):  
Jizhen Lin ◽  
Youngki Kim ◽  
Frank Ondrey ◽  
Chris Lees ◽  
Steven K. Juhn
Keyword(s):  
Arachidonic Acid ◽  
Epithelial Cells ◽  
Middle Ear ◽  
Platelet Activating Factor ◽  
Lipoxygenase Inhibitor ◽  
Lipoxygenase Inhibition ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites ◽  
Glycoprotein Secretion

Lipoxygenase is an enzyme that metabolizes arachidonic acid down to leukotrienes. Recent studies have shown that the enzyme is implicated in mucous glycoprotein (MGP) secretion stimulated by inflammatory mediators in the airways, suggesting its possible role in secretion of MGP from middle ear epithelial cells. To investigate a correlation between MGP secretion and the arachidonic acid metabolites, we examined the effects of nordihydroguaretic acid (NDGA, both a cyclooxygenase and lipoxygenase inhibitor), low-dose indomethacin (an inhibitor of cyclooxygenase), and A63162 (an inhibitor of lipoxygenase) on MGP secretion in cultured chinchilla middle ear epithelial cells. It was found that lipoxygenase inhibition led to reduction of MGP secretion from cultured chinchilla middle ear epithelial cells, while cyclooxygenase inhibition did not. Both cyclooxygenase and lipoxygenase inhibition resulted in profound blockage of MGP secretion in baseline and platelet activating factor-stimulated MGP secretion. It was concluded, therefore, that MGP secretion was linked to arachidonic acid metabolites, especially lipoxygenase products.

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