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*
Speros P. Martel Laboratory of Leukocyte Biology, Department of Pediatrics,
Department of Molecular and Human Genetics, and
Department of Medicine, Baylor College of Medicine, Houston, TX 77030;
§
Institute of Biosciences and Bioengineering, Rice University, Houston, TX;
¶
Department of Comparative Medicine, University of Alabama, Birmingham, AL 35294; and
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Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110
To differentiate the unique and overlapping functions of LFA-1 and
Mac-1, LFA-1-deficient mice were developed by targeted homologous
recombination in embryonic stem cells, and neutrophil function was
compared in vitro and in vivo with Mac-1-deficient, CD18-deficient, and
wild-type mice. LFA-1-deficient mice exhibit leukocytosis but do not
develop spontaneous infections, in contrast to CD18-deficient mice.
After zymosan-activated serum stimulation, LFA-1-deficient neutrophils
demonstrated activation, evidenced by up-regulation of surface Mac-1,
but did not show increased adhesion to purified ICAM-1 or endothelial
cells, similar to CD18-deficient neutrophils. Adhesion of
Mac-1-deficient neutrophils significantly increased with stimulation,
although adhesion was lower than for wild-type neutrophils. Evaluation
of the strength of adhesion through LFA-1, Mac-1, and CD18 indicated a
marked reduction in firm attachment, with increasing shear stress in
LFA-1-deficient neutrophils, similar to CD18-deficient neutrophils, and
only a modest reduction in Mac-1-deficient neutrophils. Leukocyte
influx in a subcutaneous air pouch in response to TNF-
was reduced
by 67% and 59% in LFA-1- and CD18-deficient mice but increased by
198% in Mac-1-deficient mice. Genetic deficiencies demonstrate that
both LFA-1 and Mac-1 contribute to adhesion of neutrophils to
endothelial cells and ICAM-1, but adhesion through LFA-1 overshadows
the contribution from Mac-1. Neutrophil extravasation in response to
TNF- in LFA-1-deficient mice dramatically decreased, whereas
neutrophil extravasation in Mac-1-deficient mice markedly
increased.
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R. B. Henderson, L. H.K. Lim, P. A. Tessier, F. N.E. Gavins, M. Mathies, M. Perretti, and N. Hogg The Use of Lymphocyte Function-Associated Antigen (Lfa)-1-Deficient Mice to Determine the Role of Lfa-1, Mac-1, and {alpha}4 Integrin in the Inflammatory Response of Neutrophils J. Exp. Med., July 16, 2001; 194(2): 219 - 226. [Abstract] [Full Text] [PDF]
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J. E. Prince, C. F. Brayton, M. C. Fossett, J. A. Durand, S. L. Kaplan, C. W. Smith, and C. M. Ballantyne The Differential Roles of LFA-1 and Mac-1 in Host Defense Against Systemic Infection with Streptococcus pneumoniae J. Immunol., June 15, 2001; 166(12): 7362 - 7369. [Abstract] [Full Text] [PDF]
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S. Tyagi, L. B. Klickstein, and A. Nicholson-Weller C5a-stimulated human neutrophils use a subset of {beta}2 integrins to support the adhesion-dependent phase of superoxide production J. Leukoc. Biol., November 1, 2000; 68(5): 679 - 686. [Abstract] [Full Text]
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F. Leite, J. F. Brown, M. J. Sylte, R. E. Briggs, and C. J. Czuprynski Recombinant Bovine Interleukin-1beta Amplifies the Effects of Partially Purified Pasteurella haemolytica Leukotoxin on Bovine Neutrophils in a beta 2-Integrin-Dependent Manner Infect. Immun., October 1, 2000; 68(10): 5581 - 5586. [Abstract] [Full Text] [PDF]
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C. W. Smith Introduction: functional polarity of motile neutrophils Blood, April 15, 2000; 95(8): 2459 - 2461. [Full Text] [PDF]
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R. A. Bowden, Z.-M. Ding, E. M. Donnachie, T. K. Petersen, L. H. Michael, C. M. Ballantyne, and A. R. Burns Role of {alpha}4 Integrin and VCAM-1 in CD18-Independent Neutrophil Migration Across Mouse Cardiac Endothelium Circ. Res., March 22, 2002; 90(5): 562 - 569. [Abstract] [Full Text] [PDF]
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