Journal of Leukocyte Biology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Originally published online as doi:10.1189/jlb.0607344 on October 10, 2007

Published online before print October 10, 2007
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jlb.0607344v1
83/1/1    most recent
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 Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Barthel, S. R.
Right arrow Articles by Mosher, D. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Barthel, S. R.
Right arrow Articles by Mosher, D. F.
(Journal of Leukocyte Biology. 2008;83:1-12.)
© 2008 by Society for Leukocyte Biology

Roles of integrin activation in eosinophil function and the eosinophilic inflammation of asthma

Steven R. Barthel*,{dagger}, Mats W. Johansson{dagger}, Dawn M. McNamee*,{dagger} and Deane F. Mosher*,{dagger},1

* Departments of Biomolecular Chemistry and
{dagger} Medicine, University of Wisconsin-Madison, Madison, Wisconsin, USA

1 Correspondence: Departments of Biomolecular Chemistry and Medicine, University of Wisconsin-Madison, 4285A Medical Sciences Center, 1300 University Avenue, Madison, WI 53706-1532, USA. E-mail: dfmosher{at}facstaff.wisc.edu

Eosinophilic inflammation is a characteristic feature of asthma. Integrins are highly versatile cellular receptors that regulate extravasation of eosinophils from the postcapillary segment of the bronchial circulation to the airway wall and airspace. Such movement into the asthmatic lung is described as a sequential, multistep paradigm, whereby integrins on circulating eosinophils become activated, eosinophils tether in flow and roll on bronchial endothelial cells, integrins on rolling eosinophils become further activated as a result of exposure to cytokines, eosinophils arrest firmly to adhesive ligands on activated endothelium, and eosinophils transmigrate to the airway in response to chemoattractants. Eosinophils express seven integrin heterodimeric adhesion molecules: {alpha}4β1 (CD49d/29), {alpha}6β1 (CD49f/29), {alpha}Mβ2 (CD11b/18), {alpha}Lβ2 (CD11a/18), {alpha}Xβ2 (CD11c/18), {alpha}Dβ2 (CD11d/18), and {alpha}4β7 (CD49d/β7). The role of these integrins in eosinophil recruitment has been elucidated by major advances in the understanding of integrin structure, integrin function, and modulators of integrins. Such findings have been facilitated by cellular experiments of eosinophils in vitro, studies of allergic asthma in humans and animal models in vivo, and crystal structures of integrins. Here, we elaborate on how integrins cooperate to mediate eosinophil movement to the asthmatic airway. Antagonists that target integrins represent potentially promising therapies in the treatment of asthma.

Key Words: cytokine • extravasation • podosome • recruitment • VCAM-1




This article has been cited by other articles:


Home page
 J. Immunol.Home page
M. W. Johansson, E. A. B. Kelly, W. W. Busse, N. N. Jarjour, and D. F. Mosher
Up-Regulation and Activation of Eosinophil Integrins in Blood and Airway after Segmental Lung Antigen Challenge
J. Immunol., June 1, 2008; 180(11): 7622 - 7635.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2008 by the Society for Leukocyte Biology.