Oxygen radical production by alveolar inflammatory cells in idiopathic pulmonary fibrosis

J. Strausz, J. Muller-Quernheim, H. Steppling, R. Ferlinz

Research output: Contribution to journalArticle

118 Citations (Scopus)

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic inflammatory interstitial lung disease characterized by the accumulation of alveolar macrophages (AMs) and neutrophils in the lower respiratory tract, parenchymal cell injury, and fibrosis of the alveolar structure. Reactive oxygen intermediates (ROI) are claimed to be a major cause of tissue damage in IPF; however, the source of ROI has not been unequivocally identified. AMs, as well as neutrophils, are capable of releasing these agents. The contributions of these possible sources are not known. To address this question, we evaluated the spontaneous and stimulated (PMA or zymosan) ROI release of total bronchoalveolar cells and isolated AMs in 14 patients with IPF by means of luminol-enhanced chemiluminescence. Bronchoalveolar lavage (BAL) cells from 17 individuals without any signs of inflammation served as controls. In comparison with the controls, the spontaneous as well as the stimulated ROI release of total BAL cells in IPF are markedly increased (20,736.9 ± 5,079.3 versus 2,509.5 ± 300.6 counts/10 s/2 · 105 cells, spontaneously, IPF versus control; 106,819.3 ± 33,802.8 versus 8,919 ± 1,357.9 PMA induced; 41,597.1 ± 8,442.6 versus 6,223.8 ± 1,025.1 zymosan induced, p <0.001). Measurement of the ROI release of purified AMs revealed that these cells produce the bulk part of ROI released by BAL cells (84%). In spite of the fact that, on a per cell basis, the ROI release of neutrophils is 1.7-fold of that of AMs, there is no correlation between the ROI production of total BAL cells and the percentage of neutrophils in BAL, demonstrating a minor role of these cells in the generation of the total ROI burden in IPF. Additionally, it was not possible to suppress the ROI release by 10-6 M prednisolone; however, some cases of clinically effective therapy with prednisolone resulted in a marked decrease of the ROI burden. Our results demonstrate that in IPF, AMs and neutrophils produce heigtened amounts of ROI; the most important source, however, are AMs.

Original languageEnglish
Pages (from-to)124-128
Number of pages5
JournalAmerican Review of Respiratory Disease
Volume141
Issue number1
Publication statusPublished - 1990

Fingerprint

Alveolar Epithelial Cells
Idiopathic Pulmonary Fibrosis
Reactive Oxygen Species
Oxygen
Alveolar Macrophages
Bronchoalveolar Lavage
Neutrophils
Zymosan
Prednisolone
Luminol
Interstitial Lung Diseases
Luminescence
Respiratory System
Fibrosis

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Oxygen radical production by alveolar inflammatory cells in idiopathic pulmonary fibrosis. / Strausz, J.; Muller-Quernheim, J.; Steppling, H.; Ferlinz, R.

In: American Review of Respiratory Disease, Vol. 141, No. 1, 1990, p. 124-128.

Research output: Contribution to journalArticle

Strausz, J. ; Muller-Quernheim, J. ; Steppling, H. ; Ferlinz, R. / Oxygen radical production by alveolar inflammatory cells in idiopathic pulmonary fibrosis. In: American Review of Respiratory Disease. 1990 ; Vol. 141, No. 1. pp. 124-128.
@article{944c8d1f3e154c8a9d9783ca3d0537e6,
title = "Oxygen radical production by alveolar inflammatory cells in idiopathic pulmonary fibrosis",
abstract = "Idiopathic pulmonary fibrosis (IPF) is a chronic inflammatory interstitial lung disease characterized by the accumulation of alveolar macrophages (AMs) and neutrophils in the lower respiratory tract, parenchymal cell injury, and fibrosis of the alveolar structure. Reactive oxygen intermediates (ROI) are claimed to be a major cause of tissue damage in IPF; however, the source of ROI has not been unequivocally identified. AMs, as well as neutrophils, are capable of releasing these agents. The contributions of these possible sources are not known. To address this question, we evaluated the spontaneous and stimulated (PMA or zymosan) ROI release of total bronchoalveolar cells and isolated AMs in 14 patients with IPF by means of luminol-enhanced chemiluminescence. Bronchoalveolar lavage (BAL) cells from 17 individuals without any signs of inflammation served as controls. In comparison with the controls, the spontaneous as well as the stimulated ROI release of total BAL cells in IPF are markedly increased (20,736.9 ± 5,079.3 versus 2,509.5 ± 300.6 counts/10 s/2 · 105 cells, spontaneously, IPF versus control; 106,819.3 ± 33,802.8 versus 8,919 ± 1,357.9 PMA induced; 41,597.1 ± 8,442.6 versus 6,223.8 ± 1,025.1 zymosan induced, p <0.001). Measurement of the ROI release of purified AMs revealed that these cells produce the bulk part of ROI released by BAL cells (84{\%}). In spite of the fact that, on a per cell basis, the ROI release of neutrophils is 1.7-fold of that of AMs, there is no correlation between the ROI production of total BAL cells and the percentage of neutrophils in BAL, demonstrating a minor role of these cells in the generation of the total ROI burden in IPF. Additionally, it was not possible to suppress the ROI release by 10-6 M prednisolone; however, some cases of clinically effective therapy with prednisolone resulted in a marked decrease of the ROI burden. Our results demonstrate that in IPF, AMs and neutrophils produce heigtened amounts of ROI; the most important source, however, are AMs.",
author = "J. Strausz and J. Muller-Quernheim and H. Steppling and R. Ferlinz",
year = "1990",
language = "English",
volume = "141",
pages = "124--128",
journal = "American Journal of Respiratory and Critical Care Medicine",
issn = "1073-449X",
publisher = "American Thoracic Society",
number = "1",

}

TY - JOUR

T1 - Oxygen radical production by alveolar inflammatory cells in idiopathic pulmonary fibrosis

AU - Strausz, J.

AU - Muller-Quernheim, J.

AU - Steppling, H.

AU - Ferlinz, R.

PY - 1990

Y1 - 1990

N2 - Idiopathic pulmonary fibrosis (IPF) is a chronic inflammatory interstitial lung disease characterized by the accumulation of alveolar macrophages (AMs) and neutrophils in the lower respiratory tract, parenchymal cell injury, and fibrosis of the alveolar structure. Reactive oxygen intermediates (ROI) are claimed to be a major cause of tissue damage in IPF; however, the source of ROI has not been unequivocally identified. AMs, as well as neutrophils, are capable of releasing these agents. The contributions of these possible sources are not known. To address this question, we evaluated the spontaneous and stimulated (PMA or zymosan) ROI release of total bronchoalveolar cells and isolated AMs in 14 patients with IPF by means of luminol-enhanced chemiluminescence. Bronchoalveolar lavage (BAL) cells from 17 individuals without any signs of inflammation served as controls. In comparison with the controls, the spontaneous as well as the stimulated ROI release of total BAL cells in IPF are markedly increased (20,736.9 ± 5,079.3 versus 2,509.5 ± 300.6 counts/10 s/2 · 105 cells, spontaneously, IPF versus control; 106,819.3 ± 33,802.8 versus 8,919 ± 1,357.9 PMA induced; 41,597.1 ± 8,442.6 versus 6,223.8 ± 1,025.1 zymosan induced, p <0.001). Measurement of the ROI release of purified AMs revealed that these cells produce the bulk part of ROI released by BAL cells (84%). In spite of the fact that, on a per cell basis, the ROI release of neutrophils is 1.7-fold of that of AMs, there is no correlation between the ROI production of total BAL cells and the percentage of neutrophils in BAL, demonstrating a minor role of these cells in the generation of the total ROI burden in IPF. Additionally, it was not possible to suppress the ROI release by 10-6 M prednisolone; however, some cases of clinically effective therapy with prednisolone resulted in a marked decrease of the ROI burden. Our results demonstrate that in IPF, AMs and neutrophils produce heigtened amounts of ROI; the most important source, however, are AMs.

AB - Idiopathic pulmonary fibrosis (IPF) is a chronic inflammatory interstitial lung disease characterized by the accumulation of alveolar macrophages (AMs) and neutrophils in the lower respiratory tract, parenchymal cell injury, and fibrosis of the alveolar structure. Reactive oxygen intermediates (ROI) are claimed to be a major cause of tissue damage in IPF; however, the source of ROI has not been unequivocally identified. AMs, as well as neutrophils, are capable of releasing these agents. The contributions of these possible sources are not known. To address this question, we evaluated the spontaneous and stimulated (PMA or zymosan) ROI release of total bronchoalveolar cells and isolated AMs in 14 patients with IPF by means of luminol-enhanced chemiluminescence. Bronchoalveolar lavage (BAL) cells from 17 individuals without any signs of inflammation served as controls. In comparison with the controls, the spontaneous as well as the stimulated ROI release of total BAL cells in IPF are markedly increased (20,736.9 ± 5,079.3 versus 2,509.5 ± 300.6 counts/10 s/2 · 105 cells, spontaneously, IPF versus control; 106,819.3 ± 33,802.8 versus 8,919 ± 1,357.9 PMA induced; 41,597.1 ± 8,442.6 versus 6,223.8 ± 1,025.1 zymosan induced, p <0.001). Measurement of the ROI release of purified AMs revealed that these cells produce the bulk part of ROI released by BAL cells (84%). In spite of the fact that, on a per cell basis, the ROI release of neutrophils is 1.7-fold of that of AMs, there is no correlation between the ROI production of total BAL cells and the percentage of neutrophils in BAL, demonstrating a minor role of these cells in the generation of the total ROI burden in IPF. Additionally, it was not possible to suppress the ROI release by 10-6 M prednisolone; however, some cases of clinically effective therapy with prednisolone resulted in a marked decrease of the ROI burden. Our results demonstrate that in IPF, AMs and neutrophils produce heigtened amounts of ROI; the most important source, however, are AMs.

UR - http://www.scopus.com/inward/record.url?scp=0025019279&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025019279&partnerID=8YFLogxK

M3 - Article

C2 - 2297170

AN - SCOPUS:0025019279

VL - 141

SP - 124

EP - 128

JO - American Journal of Respiratory and Critical Care Medicine

JF - American Journal of Respiratory and Critical Care Medicine

SN - 1073-449X

IS - 1

ER -