The JI PBL Intereron Source
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     
 


The Journal of Immunology, 1976, 117: 1356-1362.
Copyright © 1976 by The American Association of Immunologists, Inc.

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Paterson, N. A. M.
Right arrow Articles by Austen, K. F.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Paterson, N. A. M.
Right arrow Articles by Austen, K. F.

Release of Chemical Mediators from Partially Purified Human Lung Mast Cells1

Nigel A. M. Paterson2, Stephen I. Wasserman3, Jonathan W. Said and K. Frank Austen

Departments of Medicine and Pathology, Harvard Medical School; the Department of Medicine, Robert B. Brigham Hospital, and the Department of Pathology, Peter Bent Brigham Hospital, Boston, Massachusetts

Abstract

Human lung mast cells dispersed by enzymatic digestion of human lung fragments were concentrated to greater than 50% purity by sedimentation in isopycnic and velocity gradients. The dispersed lung mast cells had a characteristic ultrastructural appearance including granules with a scroll or reticular structure surrounded by perigranular membranes. Histamine and preformed eosinophilotactic activity sedimented with the mast cells on isopycnic gradients, and the mast cells and these mediators were separated from the bulk of the other lung cells after velocity gradient sedimentation. The histamine content of isolated lung mast cells was calculated to range from 1.0 to 5.5 pg/cell. The quantity of SRS-A generated with anti-IgE or specific antigen was relatively limited but confined to the mast cell-rich fractions and associated with the release of histamine and eosinophilotactic activity.

Footnotes

1 This work was supported by Grants AI-07722, AI-10356, and HL-17382 from the National Institutes of Health, Bethesda, Maryland.

2 Fellow of the Medical Research Council, Canada.

3 Research Fellow of The Arthritis Foundation.




This article has been cited by other articles:


Home page
J. Immunol.Home page
C. Taube, N. Miyahara, V. Ott, B. Swanson, K. Takeda, J. Loader, L. D. Shultz, A. M. Tager, A. D. Luster, A. Dakhama, et al.
The Leukotriene B4 Receptor (BLT1) Is Required for Effector CD8+ T Cell-Mediated, Mast Cell-Dependent Airway Hyperresponsiveness.
J. Immunol., March 1, 2006; 176(5): 3157 - 3164.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
B. L. Diaz, H. Fujishima, Y. Kanaoka, Y. Urade, and J. P. Arm
Regulation of Prostaglandin Endoperoxide Synthase-2 and IL-6 Expression in Mouse Bone Marrow-Derived Mast Cells by Exogenous But Not Endogenous Prostanoids
J. Immunol., February 1, 2002; 168(3): 1397 - 1404.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
H. Ochi, N. H. De Jesus, F. H. Hsieh, K. F. Austen, and J. A. Boyce
IL-4 and -5 prime human mast cells for different profiles of IgE-dependent cytokine production
PNAS, September 12, 2000; 97(19): 10509 - 10513.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1976 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1976 by The American Association of Immunologists, Inc. All rights reserved.