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Research Article Free access | 10.1172/JCI107735

Increased Adenosine Triphosphatase in Leukocytes of Asthmatic Children

Ronald G. Coffey, John W. Hadden, and Elliott Middleton Jr.

National Asthma Center, Denver, Colorado 80204

Memorial Sloan-Kettering Cancer Center, New York 10021

Find articles by Coffey, R. in: PubMed | Google Scholar

National Asthma Center, Denver, Colorado 80204

Memorial Sloan-Kettering Cancer Center, New York 10021

Find articles by Hadden, J. in: PubMed | Google Scholar

National Asthma Center, Denver, Colorado 80204

Memorial Sloan-Kettering Cancer Center, New York 10021

Find articles by Middleton, E. in: PubMed | Google Scholar

Published July 1, 1974 - More info

Published in Volume 54, Issue 1 on July 1, 1974
J Clin Invest. 1974;54(1):138–146. https://doi.org/10.1172/JCI107735.
© 1974 The American Society for Clinical Investigation
Published July 1, 1974 - Version history
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Abstract

Adenosine triphosphatase (ATPase) activities were compared in leukocytes of asthmatic and nonasthmatic children. Both Mg2+- and Ca2+-dependent ATPase activities were significantly elevated in two membrane fractions (59 to 66%) and in a superntant fraction (68 to 72%) prepared from sonicated leukocytes of asthmatic subjects. Intact cell surface or ecto ATPase was also elevated (67 to 76%) in asthmatic leukocytes. Alternate day glucocorticosteroid therapy was associated with leukocyte ATPase activities intermediate between those for asthmatics not receiving steroids and for nonasthmatic control subjects. Incubation of normal leukocytes with 10-8 M hydrocortisone or leukocyte membranes with 10-4-10-3 M hydrocortisone in vitro also resulted in decreased ATPase activities. The elevated leukocyte ATPase activities appear to relate to the adrenergic imbalance in asthma previously characterized by reduced beta adrenergic responsiveness of adenylate cyclase and suggest the possibility of more than one enzymatic abnormality intrinsic to the asthmatic condition.

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