Effects of trauma on leukocyte intercellular adhesion molecule-1, CD11b, and CD18 expressions

G. Scannell, K. Waxman, N. D. Vaziri, J. Zhang, C. J. Kaupke, M. Jalali, C. Hect, Richard Mullins

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Background: During traumatic injury, a multitude of events, including ischemia, may cause leukocyte adhesion and margination. In this study, alterations of surface receptors involved in leukocyte adhesion were studied in traumatized patients. In an attempt to discern the role of hypoxia, additional experiments were conducted in which normal human leukocytes were subjected to hypoxic stress in vitro. Methods: Venous blood was obtained from 10 trauma patients within 2 hours of blunt injury (mean Injury Severity Score of 17 ± 8) and from 8 normal volunteers (controls). Leukocytes were isolated from patients and controls. To assess the effect of hypoxia, normal leukocytes were placed in hermetically sealed environments containing 100% nitrogen. All leukocytes were labeled with phycoerythrin- or fluorescein- bound monoclonal antibodies to intercellular adhesion molecule-1 (ICAM-1), or to integrins CD18 and CD11b. Receptor concentration was measured by flow cytometry. Results were expressed as percentage of receptor-positive cells (%) and mean fluorescence channel units, which directly correlate with monoclonal antibody cell surface density. Significance of differences was tested by analysis of variance/Kruskal-Wallis test. Results: Compared with the normal controls, circulating leukocytes obtained from traumatized patients showed decreased expression of ICAM-1, CD11b, and CD18 2 hours after injury. In contrast, normal leukocytes exposed to hypoxic stress in vitro exhibited a marked increase in CD11b and CD18 expression and no change in ICAM-1 expression. Conclusions: Leukocytes obtained from traumatized patients showed a significant decrease in cell surface expression of adhesion receptors. This phenomenon is unlikely to be a direct consequence of hypoxia alone, because exposure to isolated hypoxia in vitro actually increased expression of CD11b and CD18.

Original languageEnglish (US)
Pages (from-to)641-644
Number of pages4
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume39
Issue number4
DOIs
StatePublished - 1995
Externally publishedYes

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Cell Adhesion Molecules
Intercellular Adhesion Molecule-1
Leukocytes
Wounds and Injuries
Monoclonal Antibodies
Phycoerythrin
Nonpenetrating Wounds
Injury Severity Score
Fluorescein
Integrins
Analysis of Variance
Healthy Volunteers
Flow Cytometry
Nitrogen
Ischemia
Cell Count
Fluorescence
Hypoxia

ASJC Scopus subject areas

  • Surgery

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Effects of trauma on leukocyte intercellular adhesion molecule-1, CD11b, and CD18 expressions. / Scannell, G.; Waxman, K.; Vaziri, N. D.; Zhang, J.; Kaupke, C. J.; Jalali, M.; Hect, C.; Mullins, Richard.

In: Journal of Trauma - Injury, Infection and Critical Care, Vol. 39, No. 4, 1995, p. 641-644.

Research output: Contribution to journalArticle

Scannell, G. ; Waxman, K. ; Vaziri, N. D. ; Zhang, J. ; Kaupke, C. J. ; Jalali, M. ; Hect, C. ; Mullins, Richard. / Effects of trauma on leukocyte intercellular adhesion molecule-1, CD11b, and CD18 expressions. In: Journal of Trauma - Injury, Infection and Critical Care. 1995 ; Vol. 39, No. 4. pp. 641-644.
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abstract = "Background: During traumatic injury, a multitude of events, including ischemia, may cause leukocyte adhesion and margination. In this study, alterations of surface receptors involved in leukocyte adhesion were studied in traumatized patients. In an attempt to discern the role of hypoxia, additional experiments were conducted in which normal human leukocytes were subjected to hypoxic stress in vitro. Methods: Venous blood was obtained from 10 trauma patients within 2 hours of blunt injury (mean Injury Severity Score of 17 ± 8) and from 8 normal volunteers (controls). Leukocytes were isolated from patients and controls. To assess the effect of hypoxia, normal leukocytes were placed in hermetically sealed environments containing 100{\%} nitrogen. All leukocytes were labeled with phycoerythrin- or fluorescein- bound monoclonal antibodies to intercellular adhesion molecule-1 (ICAM-1), or to integrins CD18 and CD11b. Receptor concentration was measured by flow cytometry. Results were expressed as percentage of receptor-positive cells ({\%}) and mean fluorescence channel units, which directly correlate with monoclonal antibody cell surface density. Significance of differences was tested by analysis of variance/Kruskal-Wallis test. Results: Compared with the normal controls, circulating leukocytes obtained from traumatized patients showed decreased expression of ICAM-1, CD11b, and CD18 2 hours after injury. In contrast, normal leukocytes exposed to hypoxic stress in vitro exhibited a marked increase in CD11b and CD18 expression and no change in ICAM-1 expression. Conclusions: Leukocytes obtained from traumatized patients showed a significant decrease in cell surface expression of adhesion receptors. This phenomenon is unlikely to be a direct consequence of hypoxia alone, because exposure to isolated hypoxia in vitro actually increased expression of CD11b and CD18.",
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AU - Scannell, G.

AU - Waxman, K.

AU - Vaziri, N. D.

AU - Zhang, J.

AU - Kaupke, C. J.

AU - Jalali, M.

AU - Hect, C.

AU - Mullins, Richard

PY - 1995

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N2 - Background: During traumatic injury, a multitude of events, including ischemia, may cause leukocyte adhesion and margination. In this study, alterations of surface receptors involved in leukocyte adhesion were studied in traumatized patients. In an attempt to discern the role of hypoxia, additional experiments were conducted in which normal human leukocytes were subjected to hypoxic stress in vitro. Methods: Venous blood was obtained from 10 trauma patients within 2 hours of blunt injury (mean Injury Severity Score of 17 ± 8) and from 8 normal volunteers (controls). Leukocytes were isolated from patients and controls. To assess the effect of hypoxia, normal leukocytes were placed in hermetically sealed environments containing 100% nitrogen. All leukocytes were labeled with phycoerythrin- or fluorescein- bound monoclonal antibodies to intercellular adhesion molecule-1 (ICAM-1), or to integrins CD18 and CD11b. Receptor concentration was measured by flow cytometry. Results were expressed as percentage of receptor-positive cells (%) and mean fluorescence channel units, which directly correlate with monoclonal antibody cell surface density. Significance of differences was tested by analysis of variance/Kruskal-Wallis test. Results: Compared with the normal controls, circulating leukocytes obtained from traumatized patients showed decreased expression of ICAM-1, CD11b, and CD18 2 hours after injury. In contrast, normal leukocytes exposed to hypoxic stress in vitro exhibited a marked increase in CD11b and CD18 expression and no change in ICAM-1 expression. Conclusions: Leukocytes obtained from traumatized patients showed a significant decrease in cell surface expression of adhesion receptors. This phenomenon is unlikely to be a direct consequence of hypoxia alone, because exposure to isolated hypoxia in vitro actually increased expression of CD11b and CD18.

AB - Background: During traumatic injury, a multitude of events, including ischemia, may cause leukocyte adhesion and margination. In this study, alterations of surface receptors involved in leukocyte adhesion were studied in traumatized patients. In an attempt to discern the role of hypoxia, additional experiments were conducted in which normal human leukocytes were subjected to hypoxic stress in vitro. Methods: Venous blood was obtained from 10 trauma patients within 2 hours of blunt injury (mean Injury Severity Score of 17 ± 8) and from 8 normal volunteers (controls). Leukocytes were isolated from patients and controls. To assess the effect of hypoxia, normal leukocytes were placed in hermetically sealed environments containing 100% nitrogen. All leukocytes were labeled with phycoerythrin- or fluorescein- bound monoclonal antibodies to intercellular adhesion molecule-1 (ICAM-1), or to integrins CD18 and CD11b. Receptor concentration was measured by flow cytometry. Results were expressed as percentage of receptor-positive cells (%) and mean fluorescence channel units, which directly correlate with monoclonal antibody cell surface density. Significance of differences was tested by analysis of variance/Kruskal-Wallis test. Results: Compared with the normal controls, circulating leukocytes obtained from traumatized patients showed decreased expression of ICAM-1, CD11b, and CD18 2 hours after injury. In contrast, normal leukocytes exposed to hypoxic stress in vitro exhibited a marked increase in CD11b and CD18 expression and no change in ICAM-1 expression. Conclusions: Leukocytes obtained from traumatized patients showed a significant decrease in cell surface expression of adhesion receptors. This phenomenon is unlikely to be a direct consequence of hypoxia alone, because exposure to isolated hypoxia in vitro actually increased expression of CD11b and CD18.

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