The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article
Right arrow Full Text (PDF, 382K)
Right arrow Alert me when this article is cited
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sacchi, F.
Right arrow Articles by Hill, H. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sacchi, F.
Right arrow Articles by Hill, H. R.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Journal of Experimental Medicine, Vol 160, 1247-1252, Copyright © 1984 by Rockefeller University Press


ARTICLES

Defective membrane potential changes in neutrophils from human neonates

F Sacchi and HR Hill

In an attempt to determine the mechanism of the profound defect in chemotaxis observed in the polymorphonuclear leukocytes (PMN) of human neonates, we have examined membrane potential changes and alterations in free intracellular calcium following chemotactic factor stimulation. Following exposure to formyl-methionyl-leucyl-phenylalanine (FMLP), PMN from adult donors (11) showed a marked change in membrane potential (31%) as determined by fluorescence emission using the cyanine dye, 3-3- dipentyloxacarbocyanine [DiOC5(3)]. In marked contrast, FMLP-stimulated PMN from 10 human neonates failed to show any significant change in membrane potential (1-2%). Using the calcium-sensitive probe Quin 2/AM, FMLP induced an increase in fluorescence of up to 51% in adult PMN (10). In contrast, the change in intracellular free calcium induced in neonatal PMN was much less (32%; P less than 0.01). These results suggest that the profound defect in chemotactic responsiveness of PMN from human neonates may result from an inability of these cells to undergo changes in membrane potential following inflammatory mediator stimulation.
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS