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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6 Pt 1
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pubmed:dateCreated |
1997-2-12
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pubmed:abstractText |
The killing of metazoan parasites by eosinophils involves the activation of a respiratory burst oxidase. To investigate whether human eosinophils possess an H+ conductance that might participate in the extrusion of H+ generated by the respiratory burst, we employed the whole cell patch-clamp technique under conditions designed to isolate putative H+ currents. We observed a slow activation of outward currents by depolarizing voltage steps. The reversal potential (Erev) of the currents was a function of the H+ gradient, demonstrating that the current was carried by H+. The H+ conductance was activated by cytosolic acidification and reversibly blocked by divalent and trivalent cations. During large prolonged depolarizing voltage steps, the current activation was followed by a decrease in current. This was due to cytosolic H+ depletion, as evidenced by 1) a change in Erev and 2) a cytosolic alkalinization. We also observed a rundown of the current, possibly due to the loss of a cytosolic factor necessary for H+ current activity. An elevated pipette Ca2+ concentration (1 microM) activated the H+ conductance, suggesting that the cytosolic Ca2+ concentration is involved in the physiological regulation of H+ currents. The Ca(2+)-activated currents had properties similar to the currents observed at low Ca2+ concentrations (Erev, high-affinity block by Zn2+, kinetics of tail currents, kinetics of rundown). The Ca2+ effect might be mediated by phospholipase A2, inasmuch as 1) the currents were also activated by arachidonic acid, 2) the Ca2+ effect and the arachidonic acid effect were not additive, and 3) the Ca2+ effect, but not the arachidonic acid effect, was blocked by a phospholipase A2 inhibitor. Taken together, our results demonstrate that human eosinophils have large H+ currents that are activated by physiological intracellular signals. The electrophysiological properties of the H+ currents and their regulation strongly suggest that they participate in H+ extrusion during the respiratory burst.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Phospholipases A,
http://linkedlifedata.com/resource/pubmed/chemical/Phospholipases A2,
http://linkedlifedata.com/resource/pubmed/chemical/Protons
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
271
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
C1861-71
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:8997186-Calcium,
pubmed-meshheading:8997186-Enzyme Inhibitors,
pubmed-meshheading:8997186-Eosinophils,
pubmed-meshheading:8997186-Humans,
pubmed-meshheading:8997186-Hydrogen-Ion Concentration,
pubmed-meshheading:8997186-Ion Transport,
pubmed-meshheading:8997186-Patch-Clamp Techniques,
pubmed-meshheading:8997186-Phospholipases A,
pubmed-meshheading:8997186-Phospholipases A2,
pubmed-meshheading:8997186-Protons
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pubmed:year |
1996
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pubmed:articleTitle |
Proton currents in human eosinophils.
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pubmed:affiliation |
Department of Medicine, University Hospital, Geneva, Switzerland. schrenze@dminov1.hcuge.ch
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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