Am J Physiol Cell Physiol Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 274: C1634-C1644, 1998;
0363-6143/98 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Barnett, C. C.
Right arrow Articles by Silliman, C. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Barnett, C. C., Jr.
Right arrow Articles by Silliman, C. C.
Vol. 274, Issue 6, C1634-C1644, June 1998

ICAM-1-CD18 interaction mediates neutrophil cytotoxicity through protease release

Carlton C. Barnett Jr.1, Ernest E. Moore1, Gary W. Mierau2, David A. Partrick1, Walter L. Biffl1, David J. Elzi3, and Christopher C. Silliman3

1 Department of Surgery, Denver Health Medical Center and University of Colorado Health Sciences Center, Denver 80204; 2 Department of Pathology, Children's Hospital, Denver 80218; and 3 Bonfils Blood Center and Department of Pediatrics, University of Colorado Health Sciences Center, Denver, Colorado 80220

Interaction of the beta 2-integrin complex on the polymorphonuclear neutrophil (PMN) with intercellular adhesion molecule-1 (ICAM-1) has been implicated in PMN-mediated cytotoxicity. This study examined interaction of the CD11a, CD11b, and CD18 subunits of the beta 2-integrin with ICAM-1, transfected into Chinese hamster ovarian (CHO) cells to avoid effects of other adhesion molecules. Incubation of quiescent PMNs with wild-type and ICAM-1-transfected CHO cells produced nominal cell lysis. Similarly, when phorbol myristate acetate (PMA)-activated PMNs were incubated with wild-type CHO cells, minimal cytotoxicity was produced. However, when ICAM-1-transfected CHO cells were incubated with PMA-activated PMNs, 40% cell lysis occurred. Blockade with a monoclonal antibody (MAb) to ICAM-1 or MAbs to CD11a, CD11b, or CD18 reduced PMN-mediated cytotoxicity to baseline. To examine the role of adhesion in cytotoxicity, we studied beta 2-integrin-mediated PMN adhesion to ICAM-1-transfected CHO cells and found that MAbs for CD11a, CD11b, and CD18 all abrogated PMN cytotoxicity despite disparate effects on adhesion. To assess the role of CD18, beta 2-integrin subunits were cross-linked, and CD18 alone mediated protease release. Moreover, ICAM-1 was immunoprecipitated from transfected CHO cells and incubated with PMNs. This soluble ICAM-1 provoked elastase release, similar to PMA, which could be inhibited by MAbs to CD18 but not MAbs to other beta 2-integrin subunits. In addition, coincubation with protease inhibitors eglin C and AAPVCK reduced PMN-mediated cytotoxicity to control levels. Finally, ICAM-1-transfected CHO cells were exposed to activated PMNs from a patient with chronic granulomatous disease that caused significant cell lysis, equivalent to that of PMNs from normal donors. Collectively, these data suggest that ICAM-1 provokes PMN-mediated cytotoxicity via CD18-mediated protease release.

transfection; adhesion molecules; integrins; neutrophil degranulation


This article has been cited by other articles:


Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
P. Kodali, P. Wu, P. A. Lahiji, E. J. Brown, and J. J. Maher
ANIT toxicity toward mouse hepatocytes in vivo is mediated primarily by neutrophils via CD18
Am J Physiol Gastrointest Liver Physiol, August 1, 2006; 291(2): G355 - G363.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
C. C. Silliman, D. J. Elzi, D. R. Ambruso, R. J. Musters, C. Hamiel, R. J. Harbeck, A. J. Paterson, A. J. Bjornsen, T. H. Wyman, M. Kelher, et al.
Lysophosphatidylcholines prime the NADPH oxidase and stimulate multiple neutrophil functions through changes in cytosolic calcium
J. Leukoc. Biol., April 1, 2003; 73(4): 511 - 524.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
T. H. Wyman, A. J. Bjornsen, D. J. Elzi, C. W. Smith, K. M. England, M. Kelher, and C. C. Silliman
A two-insult in vitro model of PMN-mediated pulmonary endothelial damage: requirements for adherence and chemokine release
Am J Physiol Cell Physiol, December 1, 2002; 283(6): C1592 - C1603.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
C. C. Silliman, E. E. Moore, G. Zallen, R. Gonzalez, J. L. Johnson, D. J. Elzi, X. Meng, K. Hanasaki, J. Ishizaki, H. Arita, et al.
Presence of the M-type sPLA2 receptor on neutrophils and its role in elastase release and adhesion
Am J Physiol Cell Physiol, October 1, 2002; 283(4): C1102 - C1113.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
T. H. Wyman, C. A. Dinarello, A. Banerjee, F. Gamboni-Robertson, A. A. Hiester, K. M. England, M. Kelher, and C. C. Silliman
Physiological levels of interleukin-18 stimulate multiple neutrophil functions through p38 MAP kinase activation
J. Leukoc. Biol., August 1, 2002; 72(2): 401 - 409.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
Y. Song, L. Ao, C. D. Raeburn, C. M. Calkins, E. Abraham, A. H. Harken, and X. Meng
A low level of TNF-{alpha} mediates hemorrhage-induced acute lung injury via p55 TNF receptor
Am J Physiol Lung Cell Mol Physiol, September 1, 2001; 281(3): L677 - L684.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
K. E. WELTY-WOLF, M. S. CARRAWAY, Y.-C. T. HUANG, S. G. SIMONSON, S. P. KANTROW, T. K. KISHIMOTO, and C. A. PIANTADOSI
Antibody to Intercellular Adhesion Molecule 1 (CD54) Decreases Survival and Not Lung Injury in Baboons with Sepsis
Am. J. Respir. Crit. Care Med., March 1, 2001; 163(3): 665 - 673.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
C. M. Calkins, D. D. Bensard, J. K. Heimbach, X. Meng, B. D. Shames, E. J. Pulido, and R. C. McIntyre Jr.
L-Arginine attenuates lipopolysaccharide-induced lung chemokine production
Am J Physiol Lung Cell Mol Physiol, March 1, 2001; 280(3): L400 - L408.
[Abstract] [Full Text] [PDF]

Home page
 ChestHome page
T. Stefanec
Endothelial Apoptosis: Could It Have a Role in the Pathogenesis and Treatment of Disease?
Chest, March 1, 2000; 117(3): 841 - 854.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online