Alteration of neutrophil (PMN) function by heparin, dexamethasone, and enalapril

Julie A. Freischlag, Michael D. Colburn, William J. Quiñones-Baldrich, Wesley S. Moore

Research output: Contribution to journalArticle

Abstract

The aim of this study is to investigate the effect of a seemingly divergent class of pharmacologic agents, each having been reported to suppress intimal hyperplasia, on neutrophil (PMN) function. Human PMNs were isolated and exposed for 30 min to either saline or one of three different pharmacologic agents, each tested at three different concentrations: Group 1, saline (control, n = 14); Groups 2-4, heparin (5000 units, n = 8; 2500 units, n = 6; 1250 units, n = 6) respectively; Groups 5-7, dexamethasone (4 mg, n = 8; 2 mg, n = 6; 1 mg, n = 6), respectively; and Groups 8-10, enalapril (1.25 mg, n = 8; 0.62 mg, n = 6; 0.31 mg, n = 6). Superoxide anion production was measured by the reduction of cytochrome c in a spectrophotometric assay. Chemotaxis was evaluated by the number of PMNs migrating across a filter using a Neuro Probe chamber. Phagocytosis was determined by the ingestion of opsonized zymosan particles by PMNs. Serum obtained from each PMN donor was used both to opsonize the zymosan and as a chemoattractant in the chemotaxis assay. No agent, at any dose, significantly changed superoxide production when compared to control cells. All three agents significantly inhibited PMN chemotaxis at every dose tested (P <0.01). In the phagocytosis assay, both heparin (at high and intermediate doses) and enalapril (at all doses) significantly reduced phagocytic activity (P <0.01); however, dexamethasone (at high and intermediate doses) produced a marked stimulation (P <0.01). We conclude that: (1) in vitro incubation of PMNs with heparin and enalapril inhibits chemotaxis and phagocytosis but has no effect on the production of superoxide anion, and (2) dexamethasone also inhibits chemotaxis and has no effect on superoxide anion production but causes a marked stimulation of PMN phagocytosis.

Original languageEnglish (US)
Pages (from-to)523-529
Number of pages7
JournalJournal of Surgical Research
Volume52
Issue number5
DOIs
StatePublished - 1992
Externally publishedYes

Fingerprint

Enalapril
Chemotaxis
Dexamethasone
Heparin
Neutrophils
Phagocytosis
Superoxides
Zymosan
Tunica Intima
Chemotactic Factors
Cytochromes c
Hyperplasia
Eating
Serum

ASJC Scopus subject areas

  • Surgery

Cite this

Freischlag, J. A., Colburn, M. D., Quiñones-Baldrich, W. J., & Moore, W. S. (1992). Alteration of neutrophil (PMN) function by heparin, dexamethasone, and enalapril. Journal of Surgical Research, 52(5), 523-529. https://doi.org/10.1016/0022-4804(92)90322-Q

Alteration of neutrophil (PMN) function by heparin, dexamethasone, and enalapril. / Freischlag, Julie A.; Colburn, Michael D.; Quiñones-Baldrich, William J.; Moore, Wesley S.

In: Journal of Surgical Research, Vol. 52, No. 5, 1992, p. 523-529.

Research output: Contribution to journalArticle

Freischlag, JA, Colburn, MD, Quiñones-Baldrich, WJ & Moore, WS 1992, 'Alteration of neutrophil (PMN) function by heparin, dexamethasone, and enalapril', Journal of Surgical Research, vol. 52, no. 5, pp. 523-529. https://doi.org/10.1016/0022-4804(92)90322-Q
Freischlag, Julie A. ; Colburn, Michael D. ; Quiñones-Baldrich, William J. ; Moore, Wesley S. / Alteration of neutrophil (PMN) function by heparin, dexamethasone, and enalapril. In: Journal of Surgical Research. 1992 ; Vol. 52, No. 5. pp. 523-529.
@article{5bf986390d5e414a9db6163f353df104,
title = "Alteration of neutrophil (PMN) function by heparin, dexamethasone, and enalapril",
abstract = "The aim of this study is to investigate the effect of a seemingly divergent class of pharmacologic agents, each having been reported to suppress intimal hyperplasia, on neutrophil (PMN) function. Human PMNs were isolated and exposed for 30 min to either saline or one of three different pharmacologic agents, each tested at three different concentrations: Group 1, saline (control, n = 14); Groups 2-4, heparin (5000 units, n = 8; 2500 units, n = 6; 1250 units, n = 6) respectively; Groups 5-7, dexamethasone (4 mg, n = 8; 2 mg, n = 6; 1 mg, n = 6), respectively; and Groups 8-10, enalapril (1.25 mg, n = 8; 0.62 mg, n = 6; 0.31 mg, n = 6). Superoxide anion production was measured by the reduction of cytochrome c in a spectrophotometric assay. Chemotaxis was evaluated by the number of PMNs migrating across a filter using a Neuro Probe chamber. Phagocytosis was determined by the ingestion of opsonized zymosan particles by PMNs. Serum obtained from each PMN donor was used both to opsonize the zymosan and as a chemoattractant in the chemotaxis assay. No agent, at any dose, significantly changed superoxide production when compared to control cells. All three agents significantly inhibited PMN chemotaxis at every dose tested (P <0.01). In the phagocytosis assay, both heparin (at high and intermediate doses) and enalapril (at all doses) significantly reduced phagocytic activity (P <0.01); however, dexamethasone (at high and intermediate doses) produced a marked stimulation (P <0.01). We conclude that: (1) in vitro incubation of PMNs with heparin and enalapril inhibits chemotaxis and phagocytosis but has no effect on the production of superoxide anion, and (2) dexamethasone also inhibits chemotaxis and has no effect on superoxide anion production but causes a marked stimulation of PMN phagocytosis.",
author = "Freischlag, {Julie A.} and Colburn, {Michael D.} and Qui{\~n}ones-Baldrich, {William J.} and Moore, {Wesley S.}",
year = "1992",
doi = "10.1016/0022-4804(92)90322-Q",
language = "English (US)",
volume = "52",
pages = "523--529",
journal = "Journal of Surgical Research",
issn = "0022-4804",
publisher = "Academic Press Inc.",
number = "5",

}

TY - JOUR

T1 - Alteration of neutrophil (PMN) function by heparin, dexamethasone, and enalapril

AU - Freischlag, Julie A.

AU - Colburn, Michael D.

AU - Quiñones-Baldrich, William J.

AU - Moore, Wesley S.

PY - 1992

Y1 - 1992

N2 - The aim of this study is to investigate the effect of a seemingly divergent class of pharmacologic agents, each having been reported to suppress intimal hyperplasia, on neutrophil (PMN) function. Human PMNs were isolated and exposed for 30 min to either saline or one of three different pharmacologic agents, each tested at three different concentrations: Group 1, saline (control, n = 14); Groups 2-4, heparin (5000 units, n = 8; 2500 units, n = 6; 1250 units, n = 6) respectively; Groups 5-7, dexamethasone (4 mg, n = 8; 2 mg, n = 6; 1 mg, n = 6), respectively; and Groups 8-10, enalapril (1.25 mg, n = 8; 0.62 mg, n = 6; 0.31 mg, n = 6). Superoxide anion production was measured by the reduction of cytochrome c in a spectrophotometric assay. Chemotaxis was evaluated by the number of PMNs migrating across a filter using a Neuro Probe chamber. Phagocytosis was determined by the ingestion of opsonized zymosan particles by PMNs. Serum obtained from each PMN donor was used both to opsonize the zymosan and as a chemoattractant in the chemotaxis assay. No agent, at any dose, significantly changed superoxide production when compared to control cells. All three agents significantly inhibited PMN chemotaxis at every dose tested (P <0.01). In the phagocytosis assay, both heparin (at high and intermediate doses) and enalapril (at all doses) significantly reduced phagocytic activity (P <0.01); however, dexamethasone (at high and intermediate doses) produced a marked stimulation (P <0.01). We conclude that: (1) in vitro incubation of PMNs with heparin and enalapril inhibits chemotaxis and phagocytosis but has no effect on the production of superoxide anion, and (2) dexamethasone also inhibits chemotaxis and has no effect on superoxide anion production but causes a marked stimulation of PMN phagocytosis.

AB - The aim of this study is to investigate the effect of a seemingly divergent class of pharmacologic agents, each having been reported to suppress intimal hyperplasia, on neutrophil (PMN) function. Human PMNs were isolated and exposed for 30 min to either saline or one of three different pharmacologic agents, each tested at three different concentrations: Group 1, saline (control, n = 14); Groups 2-4, heparin (5000 units, n = 8; 2500 units, n = 6; 1250 units, n = 6) respectively; Groups 5-7, dexamethasone (4 mg, n = 8; 2 mg, n = 6; 1 mg, n = 6), respectively; and Groups 8-10, enalapril (1.25 mg, n = 8; 0.62 mg, n = 6; 0.31 mg, n = 6). Superoxide anion production was measured by the reduction of cytochrome c in a spectrophotometric assay. Chemotaxis was evaluated by the number of PMNs migrating across a filter using a Neuro Probe chamber. Phagocytosis was determined by the ingestion of opsonized zymosan particles by PMNs. Serum obtained from each PMN donor was used both to opsonize the zymosan and as a chemoattractant in the chemotaxis assay. No agent, at any dose, significantly changed superoxide production when compared to control cells. All three agents significantly inhibited PMN chemotaxis at every dose tested (P <0.01). In the phagocytosis assay, both heparin (at high and intermediate doses) and enalapril (at all doses) significantly reduced phagocytic activity (P <0.01); however, dexamethasone (at high and intermediate doses) produced a marked stimulation (P <0.01). We conclude that: (1) in vitro incubation of PMNs with heparin and enalapril inhibits chemotaxis and phagocytosis but has no effect on the production of superoxide anion, and (2) dexamethasone also inhibits chemotaxis and has no effect on superoxide anion production but causes a marked stimulation of PMN phagocytosis.

UR - http://www.scopus.com/inward/record.url?scp=0026716474&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026716474&partnerID=8YFLogxK

U2 - 10.1016/0022-4804(92)90322-Q

DO - 10.1016/0022-4804(92)90322-Q

M3 - Article

C2 - 1320173

AN - SCOPUS:0026716474

VL - 52

SP - 523

EP - 529

JO - Journal of Surgical Research

JF - Journal of Surgical Research

SN - 0022-4804

IS - 5

ER -