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Am J Physiol Heart Circ Physiol 266: H1451-H1456, 1994;
0363-6135/94 $5.00
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AJP - Heart and Circulatory Physiology, Vol 266, Issue 4 1451-H1456, Copyright © 1994 by American Physiological Society

ARTICLES

Mediation of lung neutrophil uptake after endotoxin by CD18-integrin-dependent and -independent mechanisms

B. K. McCandless, R. P. Kaufman Jr, J. A. Cooper, P. H. Neumann and A. B. Malik
Department of Physiology and Cell Biology, Albany Medical College, New York 12208.

We studied polymorphonuclear neutrophil (PMN) uptake in lungs of endotoxemic rabbits using 111In-labeled PMN and isotope imaging by gamma scintigraphy. Rabbits were challenged intravenously with 100 micrograms Escherichia coli endotoxin either 4 or 24 h before an intravenous injection of 111In-labeled PMN, which was obtained from donor rabbits. The contribution of CD18 glycoprotein (beta 2-integrin) on PMN was examined using an anti-CD18 monoclonal antibody (MAb) IB4 infused 20 min before 111In-labeled PMN injection. In control rabbits, 111In-labeled PMN uptake in lungs was maximal within 5 min [36 +/- 2% increase above baseline (+/- SE)] and then fell exponentially with a disappearance half-time (t1/2) of 10 +/- 2 min. In rabbits challenged with endotoxin for either 4 or 24 h, maximum 111In-labeled PMN lung uptake and t1/2 values increased to 52 +/- 3 and 56 +/- 3% and to 26 +/- 2 and 31 +/- 6 min, respectively. Pretreatment with MAb IB4 (0.5 mg/kg iv) did not alter the PMN uptake response and t1/2 values in the 4-h endotoxin-challenged rabbits (i.e., maximum uptake of 52 +/- 3% above baseline and t1/2 of 26 +/- 2 min), whereas MAb IB4 prevented the increases in lung PMN uptake and t1/2 in 24-h endotoxin-challenged rabbits (maximum PMN uptake of 26 +/- 5% and t1/2 of 7 +/- 3 min; P < 0.001). In contrast, the control MAb OKM-1 did not prevent lung PMN uptake and the disappearance of PMN from lungs at either times.(ABSTRACT TRUNCATED AT 250 WORDS)


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E. S. Ong, X.-P. Gao, N. Xu, D. Predescu, A. Rahman, M. T. Broman, D. H. Jho, and A. B. Malik
E. coli pneumonia induces CD18-independent airway neutrophil migration in the absence of increased lung vascular permeability
Am J Physiol Lung Cell Mol Physiol, October 1, 2003; 285(4): L879 - L888.
[Abstract] [Full Text] [PDF]


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