Cytoplasts and Mo1-deficient neutrophils pretreated with plasma and LPS induce lung injury

M. L. Wencel, M. L. Morganroth, S. O. Schoeneich, D. E. Gannon, J. Varani, R. F. Todd, U. S. Ryan, L. A. Boxer

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

We hypothesized that neutrophil adhesion and lung injury could occur independent of the surface receptor glycoprotein. Mo1 (C3bi receptor). We investigated whether preincubation of human neutrophil-derived cytoplasts (cell fragments that lack nuclei and granules and have a fixed number of surface Mo1 receptors) with plasma and lipopolysaccharide (LPS) would augment the cytoplasts' ability to cause lung injury when activated. We also investigated whether preincubating normal human neutrophils treated with anti-Mo1 antibody with plasma and LPS would increase the neutrophils' ability to adhere and cause lung injury. Human neutrophils infused into isolated salt-perfused rat lungs subsequently stimulated with phorbol 12-myristate 13-acetate (PMA) resulted in lung injury as assessed by the accumulation of 125I-bovine serum albumin in the lung parenchyma. The infusion of cytoplasts resulted in significantly less injury. Cytoplasts preincubated in 20% human plasma and LPS caused an increase in lung injury. Similarly, neutrophils treated with plasma, LPS, and anti-Mo1 antibody or neutrophils congenitally deficient in the Mo1 surface receptor and treated with plasma and LPS augmented lung injury. Plasma and LPS preincubation also increased anti-Mo1 antibody-treated neutrophil adhesion to endothelial cell monolayers after activation by PMA. Thus plasma and LPS increase adhesion and lung injury caused by neutrophils or neutrophil fragments that share defects in Mo1 receptor expression.

Original languageEnglish (US)
Pages (from-to)25/3
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume256
Issue number3
StatePublished - Jan 1 1989

Fingerprint

Lung Injury
Lipopolysaccharides
Neutrophils
Anti-Idiotypic Antibodies
Acetates
Complement C3b
Lung
Membrane Glycoproteins
Bovine Serum Albumin
Endothelial Cells
Salts
Wounds and Injuries

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Wencel, M. L., Morganroth, M. L., Schoeneich, S. O., Gannon, D. E., Varani, J., Todd, R. F., ... Boxer, L. A. (1989). Cytoplasts and Mo1-deficient neutrophils pretreated with plasma and LPS induce lung injury. American Journal of Physiology - Heart and Circulatory Physiology, 256(3), 25/3.

Cytoplasts and Mo1-deficient neutrophils pretreated with plasma and LPS induce lung injury. / Wencel, M. L.; Morganroth, M. L.; Schoeneich, S. O.; Gannon, D. E.; Varani, J.; Todd, R. F.; Ryan, U. S.; Boxer, L. A.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 256, No. 3, 01.01.1989, p. 25/3.

Research output: Contribution to journalArticle

Wencel, ML, Morganroth, ML, Schoeneich, SO, Gannon, DE, Varani, J, Todd, RF, Ryan, US & Boxer, LA 1989, 'Cytoplasts and Mo1-deficient neutrophils pretreated with plasma and LPS induce lung injury', American Journal of Physiology - Heart and Circulatory Physiology, vol. 256, no. 3, pp. 25/3.
Wencel, M. L. ; Morganroth, M. L. ; Schoeneich, S. O. ; Gannon, D. E. ; Varani, J. ; Todd, R. F. ; Ryan, U. S. ; Boxer, L. A. / Cytoplasts and Mo1-deficient neutrophils pretreated with plasma and LPS induce lung injury. In: American Journal of Physiology - Heart and Circulatory Physiology. 1989 ; Vol. 256, No. 3. pp. 25/3.
@article{f05978880445468d937dcf6bb122ad78,
title = "Cytoplasts and Mo1-deficient neutrophils pretreated with plasma and LPS induce lung injury",
abstract = "We hypothesized that neutrophil adhesion and lung injury could occur independent of the surface receptor glycoprotein. Mo1 (C3bi receptor). We investigated whether preincubation of human neutrophil-derived cytoplasts (cell fragments that lack nuclei and granules and have a fixed number of surface Mo1 receptors) with plasma and lipopolysaccharide (LPS) would augment the cytoplasts' ability to cause lung injury when activated. We also investigated whether preincubating normal human neutrophils treated with anti-Mo1 antibody with plasma and LPS would increase the neutrophils' ability to adhere and cause lung injury. Human neutrophils infused into isolated salt-perfused rat lungs subsequently stimulated with phorbol 12-myristate 13-acetate (PMA) resulted in lung injury as assessed by the accumulation of 125I-bovine serum albumin in the lung parenchyma. The infusion of cytoplasts resulted in significantly less injury. Cytoplasts preincubated in 20{\%} human plasma and LPS caused an increase in lung injury. Similarly, neutrophils treated with plasma, LPS, and anti-Mo1 antibody or neutrophils congenitally deficient in the Mo1 surface receptor and treated with plasma and LPS augmented lung injury. Plasma and LPS preincubation also increased anti-Mo1 antibody-treated neutrophil adhesion to endothelial cell monolayers after activation by PMA. Thus plasma and LPS increase adhesion and lung injury caused by neutrophils or neutrophil fragments that share defects in Mo1 receptor expression.",
author = "Wencel, {M. L.} and Morganroth, {M. L.} and Schoeneich, {S. O.} and Gannon, {D. E.} and J. Varani and Todd, {R. F.} and Ryan, {U. S.} and Boxer, {L. A.}",
year = "1989",
month = "1",
day = "1",
language = "English (US)",
volume = "256",
pages = "25/3",
journal = "American Journal of Physiology - Renal Physiology",
issn = "0363-6127",
publisher = "American Physiological Society",
number = "3",

}

TY - JOUR

T1 - Cytoplasts and Mo1-deficient neutrophils pretreated with plasma and LPS induce lung injury

AU - Wencel, M. L.

AU - Morganroth, M. L.

AU - Schoeneich, S. O.

AU - Gannon, D. E.

AU - Varani, J.

AU - Todd, R. F.

AU - Ryan, U. S.

AU - Boxer, L. A.

PY - 1989/1/1

Y1 - 1989/1/1

N2 - We hypothesized that neutrophil adhesion and lung injury could occur independent of the surface receptor glycoprotein. Mo1 (C3bi receptor). We investigated whether preincubation of human neutrophil-derived cytoplasts (cell fragments that lack nuclei and granules and have a fixed number of surface Mo1 receptors) with plasma and lipopolysaccharide (LPS) would augment the cytoplasts' ability to cause lung injury when activated. We also investigated whether preincubating normal human neutrophils treated with anti-Mo1 antibody with plasma and LPS would increase the neutrophils' ability to adhere and cause lung injury. Human neutrophils infused into isolated salt-perfused rat lungs subsequently stimulated with phorbol 12-myristate 13-acetate (PMA) resulted in lung injury as assessed by the accumulation of 125I-bovine serum albumin in the lung parenchyma. The infusion of cytoplasts resulted in significantly less injury. Cytoplasts preincubated in 20% human plasma and LPS caused an increase in lung injury. Similarly, neutrophils treated with plasma, LPS, and anti-Mo1 antibody or neutrophils congenitally deficient in the Mo1 surface receptor and treated with plasma and LPS augmented lung injury. Plasma and LPS preincubation also increased anti-Mo1 antibody-treated neutrophil adhesion to endothelial cell monolayers after activation by PMA. Thus plasma and LPS increase adhesion and lung injury caused by neutrophils or neutrophil fragments that share defects in Mo1 receptor expression.

AB - We hypothesized that neutrophil adhesion and lung injury could occur independent of the surface receptor glycoprotein. Mo1 (C3bi receptor). We investigated whether preincubation of human neutrophil-derived cytoplasts (cell fragments that lack nuclei and granules and have a fixed number of surface Mo1 receptors) with plasma and lipopolysaccharide (LPS) would augment the cytoplasts' ability to cause lung injury when activated. We also investigated whether preincubating normal human neutrophils treated with anti-Mo1 antibody with plasma and LPS would increase the neutrophils' ability to adhere and cause lung injury. Human neutrophils infused into isolated salt-perfused rat lungs subsequently stimulated with phorbol 12-myristate 13-acetate (PMA) resulted in lung injury as assessed by the accumulation of 125I-bovine serum albumin in the lung parenchyma. The infusion of cytoplasts resulted in significantly less injury. Cytoplasts preincubated in 20% human plasma and LPS caused an increase in lung injury. Similarly, neutrophils treated with plasma, LPS, and anti-Mo1 antibody or neutrophils congenitally deficient in the Mo1 surface receptor and treated with plasma and LPS augmented lung injury. Plasma and LPS preincubation also increased anti-Mo1 antibody-treated neutrophil adhesion to endothelial cell monolayers after activation by PMA. Thus plasma and LPS increase adhesion and lung injury caused by neutrophils or neutrophil fragments that share defects in Mo1 receptor expression.

UR - http://www.scopus.com/inward/record.url?scp=0024541843&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024541843&partnerID=8YFLogxK

M3 - Article

C2 - 2538083

AN - SCOPUS:0024541843

VL - 256

SP - 25/3

JO - American Journal of Physiology - Renal Physiology

JF - American Journal of Physiology - Renal Physiology

SN - 0363-6127

IS - 3

ER -