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Articles in PresS, published online ahead of print November 16, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00298.2001
Submitted on August 2, 2001
Accepted on November 13, 2001
1 Pharmacology, University of Illinois, Chicago, IL, USA
* To whom correspondence should be addressed. E-mail: arahman{at}uic.edu.
We determined the time-dependent effects of conditional expression of neutrophil inhibitory factor (NIF), a specific 41 kDa CD18 integrin antagonist, on the time course of lung PMN infiltration and vascular injury in a model of E. coli -induced sepsis in mice. Studies were made in mice transduced with pES-NIF construct (using liposomes)in which NIF cDNA was driven by the inflammation- and endothelial cell-specific E-selectin (ES) promoter. We observed the time-dependent expression of NIF in pulmonary vascular endothelium that paralleled the E-selectin expression. Expression of both was evident at 1 hr after E. coli challenge, peaked at 3-6 hr, and returned to basal level within 48 hr. We observed that increases in PMN uptake and transalveolar PMN migration induced by E. coli challenge were reversed in a time-dependent manner following NIF expression in mice. NIF expression also prevented the progression of lung vascular injury and edema formation following E. coli challenge. Thus, the conditional expression of NIF using the E-selectin promoter can reverse in a time-dependent manner lung PMN infiltration and vascular injury induced by Gram negative sepsis. The results support the model that initial engagement of CD18 integrins enables the further recruitment of additional PMN into lung tissues such that PMN continue to sequester and migrate following E. coli challenge.
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