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1 Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, VA, USA
2 Cardiovascular Research Center, University of Virginia, Charlottesville, VA, USA
3 Cardiovascular Research Center, University of Virginia, Charlottesville, VA, USA; Biomedical Engineering Department, University of Virginia, Charlottesville, VA, USA
4 Flow Cytometry Core Facility, University of Virginia, Charlottesville, VA, USA
5 Division of Pulmonary and Critical Care Medicine, University of Virginia, Charlottesville, VA, USA
6 Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, VA, USA; Cardiovascular Research Center, University of Virginia, Charlottesville, VA, USA; Biomedical Engineering Department, University of Virginia, Charlottesville, VA, USA
* To whom correspondence should be addressed. E-mail: klausley{at}virginia.edu.
Neutrophil recruitment into lung constitutes a major response to airborne endotoxins. In many tissues endothelial Intercellular Adhesion Molecule-1 (ICAM-1) interacts with Lymphocyte Function Associated Antigen-1 (LFA-1) on neutrophils, and this interaction plays a critical role in neutrophil recruitment. There are conflicting reports about the role of ICAM-1 in neutrophil recruitment into lungs. We studied neutrophil recruitment into alveolar space in a murine model of aerosolized LPS-induced lung inflammation. LPS induces at least a 100 fold increase in neutrophil numbers in alveolar space, as determined by flow cytometry of broncho-alveolar lavage fluid. Neutrophil recruitment was reduced by 54 % in ICAM-1 null mice and by 45 % in LFA-1 null mice. In wild type mice treated with anti ICAM-1 and anti LFA-1 antibodies, there was 51 % and 58 % reduction in the neutrophil recruitment, respectively. In chimeric mice, generated by the transplantation of mixtures of bone marrows from LFA-1 null and wild type mice, the normalized recruitment of LFA-1 null neutrophils was reduced by 60 % compared to wild type neutrophils. Neither the treatment of ICAM-1 null mice with a function-blocking antibody to LFA-1 nor the treatment of LFA-1 null mice with anti ICAM-1 antibody resulted in further reduction in the recruitment compared to untreated ICAM-1 null and LFA-1 null mice. We conclude that ICAM-1 and LFA-1 play critical roles in the recruitment of neutrophils into the alveolar space in aerosolized LPS-induced lung inflammation, and LFA-1 serves as a ligand of ICAM-1 in the lung.
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