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Cited by 81Cell Adhesion Molecules ResearchInflammation biomarkers and pathwaysNeutrophil, Myeloperoxidase and Oxidative Mechanisms

In vivo expression of neutrophil inhibitory factor via gene transfer prevents lipopolysaccharide-induced lung neutrophil infiltration and injury by a beta2 integrin-dependent mechanism

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Zhou, M Y, Lo, S K, Bergenfeldt, M, Tiruppathi, C, Jaffe, A, Xu, N, Malik, A B·1998·Journal of Clinical Investigation
DOI 10.1172/jci407PMC PMC508832
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Abstract

The binding of beta2 (CD18) integrins on PMN cell membrane to intercellular adhesion molecule (ICAM) counter-receptors on the surface of vascular endothelial cells mediates PMN adhesion to endothelial cells. Neutrophil inhibitory factor (NIF), a 41-kD glycoprotein isolated from the canine hookworm (Ancylostoma caninum), is a beta2 integrin antagonist that inhibits PMN adhesion to endothelial cells. We transferred the NIF gene into CD1 mouse lungs by intravenous injection of cationic liposomes to study the effects of in vivo NIF expression on LPS-induced lung PMN sequestration and the development of lung injury. RT-PCR and Northern blot analysis indicated the lung-selective expression of the NIF transgene, and immunocytochemistry showed prominent NIF expression in pulmonary microvessel endothelial cells. NIF staining was also observed in intraluminal leukocytes present in pulmonary microvessels. This may be the result of NIF binding to leukocytes after its secretion from the transduced lung cells, since there was no evidence of NIF gene expression in circulating leukocytes. Pulmonary vascular NIF expression abrogated the lung tissue PMN uptake and airspace migration of PMN and prevented lung vascular injury (as measured by the lung tissue uptake of [125I]labeled albumin) after the intraperitoneal LPS challenge (200 microg/mouse). Expression of a control protein, chloramphenicol acetyltransferase (CAT), by the same strategy, had no effect on these responses. In vitro studies showed that NIF prevented mouse PMN adhesion consistent with the inhibition of lung uptake after LPS challenge in NIF transgene-expressing mice. We conclude that pulmonary vascular expression of NIF, a specific beta2 integrin- binding protein, is a potentially useful gene transfer strategy in modulating the infiltration of PMN across the alveolar-capillary epithelial barrier and in preventing lung vascular endothelial injury.

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Authors
Zhou, M. Y., Lo, S. K., Bergenfeldt, M., Tiruppathi, C., Jaffe, A., Xu, N., & Malik, A. B.
Affiliations
  • University of Illinois Chicago (US)
  • Cornell University (US)
ORCID
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1998-06-01
Volume
101
Issue
11
Pages
2427-2437
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci407
PMC
PMC508832
OpenAlex
W2010081264
Cited by
81
References
42
Citations by year
2026: 2 · 2025: 1 · 2024: 1 · 2023: 4 · 2022: 3 · 2020: 1 · 2019: 3 · 2018: 2 · 2017: 3 · 2015: 2 · 2014: 6 · 2013: 2 · 2012: 5
FWCI
2.38
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Heart Association
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (R01HL046350, HL-45638, HL 27016, HL-46350, R01HL045638)
Topics
  • Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Keywords
CD18, neutrophil adhesion, lipopolysaccharide-induced lung injury, lung neutrophil infiltration, gene transfer, cationic liposomes, ICAM, Ancylostoma caninum, alveolar-capillary barrier
MeSH terms
Animals, Cell Adhesion, Endothelium, Vascular, Glycoproteins, Lipopolysaccharides, Lung, Male, Membrane Proteins, Mice, Transgenic, Neutrophils, Helminth Proteins, Gene Transfer Techniques, CD18 Antigens, Mice

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