Abstract
In order to more fully understand the mechanisms involved in the developmental defect in polymorphonuclear leukocyte (PMN) movement in human neonates, the authors have examined several events in the activation response sequence. Chemotactic factor receptor numbers have been found to be normal on the PMNs of neonates, but chemotactic factor-induced changes in membrane potential and cyclic adenosine monophosphate concentrations were markedly decreased to absent in the neonatal cells. Because the neonatal PMN lacks the ability to deform normally, we examined the effects of a methylxanthine derivative, pentoxifylline, on the responses of neonatal cells. This agent has been reported to increase cell deformability and improve cell movement. Pentoxifylline had an effect in improving chemotactic function in the PMNs of neonates, while correcting the abnormality in membrane potential. In addition, this agent was found to enhance the movement of cell surface concanavalin A receptors after colchicine treatment. These results suggest that this developmental defect in cell activation and movement may be an abnormality that can be corrected pharmacologically.
MeSH Terms
Adenosine Triphosphate/analysis
Anesthetics, Local/pharmacology
Cell Movement
Colchicine/pharmacology
Concanavalin A/metabolism
Cyclic AMP/biosynthesis
Fetal Blood/physiology
Humans
Membrane Potentials/drug effects
N-Formylmethionine Leucyl-Phenylalanine/metabolism
Neutrophils/physiology
Pentoxifylline/pharmacology
Receptors, Formyl Peptide
Receptors, Immunologic/metabolism
Receptors, Mitogen/drug effects
Chemicals
Anesthetics, Local
Receptors, Formyl Peptide
Receptors, Immunologic
Receptors, Mitogen
Concanavalin A
N-Formylmethionine Leucyl-Phenylalanine
Adenosine Triphosphate
Cyclic AMP
Pentoxifylline
Colchicine
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Hill H R
Augustine N H
Newton J A
Shigeoka A O
Morris E
Sacchi F
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