Source:http://linkedlifedata.com/resource/pubmed/id/19197381
General Info
Affiliation
Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA. mikewang@hsph.harvard.eduAbstract
We conducted an exploratory study of genome-wide gene expression in whole blood and found that the expression of neutrophil elastase inhibitor (PI3, elafin) was down-regulated during the early phase of ARDS. Further analyses of plasma PI3 levels revealed a rapid decrease during early ARDS development. PI3 and secretory leukocyte proteinase inhibitor (SLPI) are important low-molecular-weight proteinase inhibitors produced locally at neutrophil infiltration site in the lung. In this study, we tested the hypothesis that an imbalance between neutrophil elastase (HNE) and its inhibitors in blood is related to the development of ARDS.
PMID
19197381
Publication types
Research Support, N.I.H., Extramural