Increased immunoreactive rat lung icam-1 in oleic acid-induced lung injury

Sergei Syrbu, Roger S. Thrall, Peter Wisniecki, Scott Lifchez, Henry M. Smilowitz

Research output: Contribution to journalArticle

Abstract

Levels of immunoreactive ICAM-1 in rat lung were followed during the kinetic development of acute oleic acid-induced lung injury in the rat by the ELISA assay. Significant increases in ICAM-1 immunoreactivity were found on rat lung membranes within 30 min of oleic acid injection. The increased immunoreactive ICAM-1 persisted for the duration of the study (4 h) and paralleled lung injury as measured by decreased lung compliance. Enhanced ICAM-1 immunofluorescence was also observed on cryostat sections of lungs from oleic acid-treated rats. No direct effect of oleic acid on ICAM-1 levels of cultured human umbilical vein endothelial cells or rat lung microvascular endothelial cells was observed. This suggests that either oleic acid raises rat lung ICAM-1 levels on endothelial cells by an indirect mechanism or that oleic acid increases ICAM-1 levels on other cell types, such as fibroblasts or lung epithelial cells, by direct or indirect mechanisms. Some of the increased ICAM-1 may also be due to the accumulation of ICAM-1 containing circulating leukocytes in the lung. The role of ICAM-1 in the pathophysiology of oleic acid-induced lung injury and the mechanism by which oleic acid increases ICAM-1 expression in the lung therefore remain to be defined by future experimentation.

Original languageEnglish (US)
Pages (from-to)599-616
Number of pages18
JournalExperimental Lung Research
Volume21
Issue number4
DOIs
StatePublished - 1995
Externally publishedYes

Fingerprint

Lung Injury
Intercellular Adhesion Molecule-1
Oleic Acid
Rats
Lung
Endothelial cells
Endothelial Cells
Lung Compliance
Cryostats
Human Umbilical Vein Endothelial Cells
Fibroblasts
Fluorescent Antibody Technique
Assays
Leukocytes
Epithelial Cells
Enzyme-Linked Immunosorbent Assay
Membranes
Injections
Kinetics

Keywords

  • Endothelial cells
  • ICAM-1
  • Oleic acid
  • Rat lung injury

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Molecular Biology
  • Clinical Biochemistry

Cite this

Increased immunoreactive rat lung icam-1 in oleic acid-induced lung injury. / Syrbu, Sergei; Thrall, Roger S.; Wisniecki, Peter; Lifchez, Scott; Smilowitz, Henry M.

In: Experimental Lung Research, Vol. 21, No. 4, 1995, p. 599-616.

Research output: Contribution to journalArticle

Syrbu, Sergei ; Thrall, Roger S. ; Wisniecki, Peter ; Lifchez, Scott ; Smilowitz, Henry M. / Increased immunoreactive rat lung icam-1 in oleic acid-induced lung injury. In: Experimental Lung Research. 1995 ; Vol. 21, No. 4. pp. 599-616.
@article{fe63ff99a0164c169e11aaa558213dc3,
title = "Increased immunoreactive rat lung icam-1 in oleic acid-induced lung injury",
abstract = "Levels of immunoreactive ICAM-1 in rat lung were followed during the kinetic development of acute oleic acid-induced lung injury in the rat by the ELISA assay. Significant increases in ICAM-1 immunoreactivity were found on rat lung membranes within 30 min of oleic acid injection. The increased immunoreactive ICAM-1 persisted for the duration of the study (4 h) and paralleled lung injury as measured by decreased lung compliance. Enhanced ICAM-1 immunofluorescence was also observed on cryostat sections of lungs from oleic acid-treated rats. No direct effect of oleic acid on ICAM-1 levels of cultured human umbilical vein endothelial cells or rat lung microvascular endothelial cells was observed. This suggests that either oleic acid raises rat lung ICAM-1 levels on endothelial cells by an indirect mechanism or that oleic acid increases ICAM-1 levels on other cell types, such as fibroblasts or lung epithelial cells, by direct or indirect mechanisms. Some of the increased ICAM-1 may also be due to the accumulation of ICAM-1 containing circulating leukocytes in the lung. The role of ICAM-1 in the pathophysiology of oleic acid-induced lung injury and the mechanism by which oleic acid increases ICAM-1 expression in the lung therefore remain to be defined by future experimentation.",
keywords = "Endothelial cells, ICAM-1, Oleic acid, Rat lung injury",
author = "Sergei Syrbu and Thrall, {Roger S.} and Peter Wisniecki and Scott Lifchez and Smilowitz, {Henry M.}",
year = "1995",
doi = "10.3109/01902149509031762",
language = "English (US)",
volume = "21",
pages = "599--616",
journal = "Experimental Lung Research",
issn = "0190-2148",
publisher = "Informa Healthcare",
number = "4",

}

TY - JOUR

T1 - Increased immunoreactive rat lung icam-1 in oleic acid-induced lung injury

AU - Syrbu, Sergei

AU - Thrall, Roger S.

AU - Wisniecki, Peter

AU - Lifchez, Scott

AU - Smilowitz, Henry M.

PY - 1995

Y1 - 1995

N2 - Levels of immunoreactive ICAM-1 in rat lung were followed during the kinetic development of acute oleic acid-induced lung injury in the rat by the ELISA assay. Significant increases in ICAM-1 immunoreactivity were found on rat lung membranes within 30 min of oleic acid injection. The increased immunoreactive ICAM-1 persisted for the duration of the study (4 h) and paralleled lung injury as measured by decreased lung compliance. Enhanced ICAM-1 immunofluorescence was also observed on cryostat sections of lungs from oleic acid-treated rats. No direct effect of oleic acid on ICAM-1 levels of cultured human umbilical vein endothelial cells or rat lung microvascular endothelial cells was observed. This suggests that either oleic acid raises rat lung ICAM-1 levels on endothelial cells by an indirect mechanism or that oleic acid increases ICAM-1 levels on other cell types, such as fibroblasts or lung epithelial cells, by direct or indirect mechanisms. Some of the increased ICAM-1 may also be due to the accumulation of ICAM-1 containing circulating leukocytes in the lung. The role of ICAM-1 in the pathophysiology of oleic acid-induced lung injury and the mechanism by which oleic acid increases ICAM-1 expression in the lung therefore remain to be defined by future experimentation.

AB - Levels of immunoreactive ICAM-1 in rat lung were followed during the kinetic development of acute oleic acid-induced lung injury in the rat by the ELISA assay. Significant increases in ICAM-1 immunoreactivity were found on rat lung membranes within 30 min of oleic acid injection. The increased immunoreactive ICAM-1 persisted for the duration of the study (4 h) and paralleled lung injury as measured by decreased lung compliance. Enhanced ICAM-1 immunofluorescence was also observed on cryostat sections of lungs from oleic acid-treated rats. No direct effect of oleic acid on ICAM-1 levels of cultured human umbilical vein endothelial cells or rat lung microvascular endothelial cells was observed. This suggests that either oleic acid raises rat lung ICAM-1 levels on endothelial cells by an indirect mechanism or that oleic acid increases ICAM-1 levels on other cell types, such as fibroblasts or lung epithelial cells, by direct or indirect mechanisms. Some of the increased ICAM-1 may also be due to the accumulation of ICAM-1 containing circulating leukocytes in the lung. The role of ICAM-1 in the pathophysiology of oleic acid-induced lung injury and the mechanism by which oleic acid increases ICAM-1 expression in the lung therefore remain to be defined by future experimentation.

KW - Endothelial cells

KW - ICAM-1

KW - Oleic acid

KW - Rat lung injury

UR - http://www.scopus.com/inward/record.url?scp=0029083508&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029083508&partnerID=8YFLogxK

U2 - 10.3109/01902149509031762

DO - 10.3109/01902149509031762

M3 - Article

C2 - 7588446

AN - SCOPUS:0029083508

VL - 21

SP - 599

EP - 616

JO - Experimental Lung Research

JF - Experimental Lung Research

SN - 0190-2148

IS - 4

ER -