Role of Platelet-Activating Factor in the Release of Neutrophil and Eosinophil Chemotactic Attractants from Cultured Guinea-Pig Tracheal Epithelial Cells

1995 ◽  
Vol 108 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Masafumi Arima ◽  
Ken-ichi Manaka ◽  
Takeshi Fukuda ◽  
Souhei Makino
Keyword(s):  
Epithelial Cells ◽  
Guinea Pig ◽  
Platelet Activating Factor ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

scholarly journals Characterization of specific binding sites of 3H-labelled platelet-activating factor ([3H]PAF) and a new antagonist, [3H]SR 27417, on guinea-pig tracheal epithelial cells

1992 ◽  
Vol 284 (1) ◽  
pp. 201-206 ◽  
Author(s):  
J M Herbert
Keyword(s):  
Epithelial Cells ◽  
Guinea Pig ◽  
Binding Sites ◽  
Specific Binding ◽  
Platelet Activating Factor ◽  
Tracheal Epithelial Cells ◽  
Specific Binding Sites ◽  
Paf Receptor ◽  
Tracheal Epithelial ◽  
Paf Receptor Antagonist

Binding of 3H-labelled platelet-activating factor ([3H]PAF) to guinea-pig tracheal epithelial cells was time-dependent, reversible and saturable. Scatchard analysis of the saturation-binding data indicated that [3H]PAF bound to one class of specific binding sites with high affinity (KD = 4.3 +/- 0.03 nM; Bmax. = 0.172 +/- 0.02 fmol/10(5) cells; n = 3). Unlabelled PAF competitively and selectively inhibited the specific binding of [3H]PAF with 50% inhibition at 4.8 +/- 0.07 nM (n = 3). SR 27417, the first member of a newly developed PAF antagonist series, competitively displaced [3H]PAF from its binding sites on guinea-pig tracheal epithelial cells with a Ki of 100 +/- 3 pM (n = 3). Studies carried out in parallel demonstrated that SR 27417 was 40 times more potent than C16-PAF itself and more than 100-fold as active as the best synthetic PAF-receptor antagonist yet described. [3H]SR 27417 displayed high-affinity, specific, reversible as well as saturable binding to a single class of binding sites on tracheal epithelial cells (KD = 94 +/- 7 pM; Bmax. = 0.181 +/- 0.04 fmol/10(5) cells; n = 3). C16-PAF, lyso-PAF, enantio-PAF, SR 27417 and other PAF-receptor antagonists had Ki values which were nearly identical for both [3H]PAF and [3H]SR 27417, demonstrating that in guinea-pig tracheal epithelial cells they have the same binding sites. In conclusion, these data suggest that tracheal epithelial cells contain PAF-specific receptors and indicate that SR 27417 is an extremely potent PAF-receptor antagonist, as well as being a suitable radioligand for labelling PAF receptors on intact cells.

scholarly journals Interaction of platelet-activating factor with cultured guinea pig tracheal epithelial cells

1991 ◽  
Vol 276 (3) ◽  
pp. 593-598 ◽  
Author(s):  
L Churchill ◽  
F H Chilton ◽  
D Proud
Keyword(s):  
Epithelial Cells ◽  
Guinea Pig ◽  
Platelet Activating Factor ◽  
Inflammatory Reactions ◽  
Tracheal Epithelial Cells ◽  
Enhanced Production ◽  
Chain Acyl ◽  
Lipid Product ◽  
Major Route ◽  
Tracheal Epithelial

The present study has examined the interaction of platelet-activating factor (PAF) with cultured guinea pig tracheal epithelial cells (GTE). PAF stimulated GTE to release endogenous arachidonic acid and metabolize it to prostaglandins E2 and F2 alpha (PGE2 and PGF2 alpha). Prostanoid production by GTE in response to PAF was dose-dependent (0.1-100 nM) and was maximal within 5 min. PGE2 and PGF2 alpha levels increased by 3.3 +/- 0.8 and 3.2 +/- 0.6 ng/10(6) cells respectively over basal levels in response to 100 nM-PAF. The ability of GTE to synthesize and/or catabolize PAF was also examined. GTE readily incorporated [3H]acetate into a product which migrated on t.l.c. with PAF. However, further characterization of this product suggested that label had not been incorporated into PAF, but rather that it was incorporated into another lipid product with chromatographic characteristics similar to those of PAF. In contrast, GTE readily metabolized PAF to inactive products. When [3H]PAF was incubated with GTE, 50% of the total [3H]PAF added was catabolized in approx. 15 min. The major route of catabolism of PAF by GTE was the deacetylation-reacylation pathway, which yielded 1-O-[3H]alkyl-2-acyl-sn-glycerophosphocholine. Determination of the nature of the long-chain acyl group incorporated into the sn-2 position of the newly synthesized products revealed that oleic and linoleic acids were the major fatty acids present. Taken together, these results suggest that respiratory epithelial cells respond to stimulation by PAF with enhanced production of PGE2 and PGF2 alpha, and also have the capacity to modulate inflammatory reactions in the airways by their ability to degrade this potent inflammatory mediator.

scholarly journals Prostaglandin E2 increases cyclic AMP and inhibits endothelin-1 production/secretion by guinea-pig tracheal epithelial cells through EP4 receptors

2001 ◽  
Vol 132 (5) ◽  
pp. 999-1008 ◽  
Author(s):  
Stéphane Pelletier ◽  
Jean Dubé ◽  
Annie Villeneuve ◽  
Fernand Gobeil ◽  
Quan Yang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cyclic Amp ◽  
Guinea Pig ◽  
Prostaglandin E2 ◽  
Endothelin 1 ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

Release of reactive oxygen species by guinea pig tracheal epithelial cells in vitro

1992 ◽  
Vol 262 (6) ◽  
pp. L708-L712 ◽  
Author(s):  
V. L. Kinnula ◽  
K. B. Adler ◽  
N. J. Ackley ◽  
J. D. Crapo
Keyword(s):  
Reactive Oxygen Species ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Guinea Pig ◽  
Oxygen Species ◽  
Tracheal Epithelial Cells ◽  
Kinase C ◽  
Apical Side ◽  
Tracheal Epithelial

Regulatory and stimulatory mechanisms of H2O2 release from guinea pig tracheal epithelial cells were investigated. Cells in primary culture maintained in a previously described air-liquid interface system released H2O2 to the extracellular space only from the apical side of the cells. The rate of release was 0.044 +/- 0.003 nmol.min-1.mg protein-1. H2O2 release could be stimulated significantly during a 30-min incubation period with phorbol myristate acetate (PMA) and platelet-activating factor (PAF). A stimulatory effect of PAF was achieved at concentrations greater than 100 nM and with PMA at concentrations greater than 10 ng (16 nM). When protein kinase C was inactivated with staurosporine, the responses to both PAF and PMA were abolished, whereas the cyclooxygenase inhibitor, indomethacin, did not affect H2O2 generation. When guinea pig tracheal epithelial cells were exposed to sublethal concentrations of extracellular H2O2 (30 microM), H2O2 was detoxified from both apical and basal sides, H2O2 removal being significantly more rapid from the apical side of the cells. These results suggest that tracheal epithelial cells can be stimulated to generate reactive oxygen species into the airway lumen and that this occurs in response to inflammatory mediators that act through protein kinase C. Luminal H2O2 release may have developed as a defense mechanism against microbes, and, similarly, luminal detoxification of H2O2 could represent an important mechanism of modulation of airway inflammation in response to oxidant stress.

scholarly journals Bordetella pertussis Adenylate Cyclase-Hemolysin Induces Interleukin-6 Secretion by Human Tracheal Epithelial Cells

2004 ◽  
Vol 72 (9) ◽  
pp. 5530-5533 ◽  
Author(s):  
Laurence Bassinet ◽  
Catherine Fitting ◽  
Bruno Housset ◽  
Jean-Marc Cavaillon ◽  
Nicole Guiso
Keyword(s):  
Epithelial Cells ◽  
Adenylate Cyclase ◽  
Bordetella Pertussis ◽  
Interleukin 6 ◽  
Bacterial Toxins ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

ABSTRACT After interaction with tracheal epithelial cells, Bordetella pertussis induces the secretion of interleukin-6. This secretion is dependent on the expression of adenylate cyclase-hemolysin by the bacterium but not on the expression of other characterized bacterial toxins or adhesins. This finding confirms the important role of adenylate cyclase-hemolysin in the pathogenicity of the bacterium.

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