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Proton channels, plasma membrane potential, and respiratory burst in human neutrophils
Author(s) -
Demaurex Nicolas,
Schrenzel Jacques,
Jaconi Marisa E.,
Lew Daniel P.,
Krause KarlHeinz
Publication year - 1993
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.1993.tb01613.x
Subject(s) - depolarization , nadph oxidase , respiratory burst , biophysics , chemistry , membrane potential , intracellular , cytosol , conductance , biochemistry , reactive oxygen species , biology , enzyme , mathematics , combinatorics
When confronted with invading microorganisms, neutrophils undergo a number of nearly synchronous reactions including the generation of microbicidal reactive oxygen intermediates by the NADPH oxidase. These reactions are accompanied by a slow depolarization, from resting values of – 60 mV to levels probably exceeding 0 mV. The depolarization is transient, indicating that a compensatory charge transport mechanism is activated. Activation of the oxidase system causes a massive burst of metabolic acid generation that would, if uncompensated, lower the intracellular pH of neutrophils by over 5 units, to lethal levels (pH = 2). Neutrophils must therefore possess particularly effective regulatory systems to avoid excessive cytosolic acidification. The recently described H + conductance of neutrophils may counteract both the acidification and the depolarization. Activation of the H + conductance occurs at depolarizing voltages and is promoted by cytosolic acidification, a combination that takes place during the respiratory burst. The NADPH oxidase of neutrophils is thus associated to an unusual, particularly efficient mechanism of H + export and charge compensation. The sequential activation of these two systems causes neutrophils to depolarize through the activation of an electron transport chain, and to repolarize through the activation of a H + conductance.