Priming of alveolar macrophages for interleukin-8 production in patients with idiopathic pulmonary fibrosis

H. Nakamura, S. Fujishima, Y. Waki, T. Urano, K. Sayama, F. Sakamaki, T. Terashima, K. Soejima, S. Tasaka, A. Ishizaka, T. Kawashiro, M. Kanazawa

Research output: Contribution to journalArticle

Abstract

We evaluated the contribution of interleukin-8 (IL-8) to the pathogenesis of idiopathic pulmonary fibrosis (IPF) by studying bronchoalveolar lavage fluid (BALF) in eight patients with IPF in the chronically progressive phase, five patients with IPF in the subacutely progressive phase, eight patients with sarcoidosis (SAR), and eight control (CTL) subjects. IL-8 levels were not increased in the BALF of the patients with IPF in the chronic phase (11.3 ± 8.8 pg/ml), nor in that of the SAR patients (13.8 ± 7.8 pg/ml), whereas they were increased in the BALF of patients with IPF in the subacutely progressive phase (1.93 ± 1.10 ng/ml). We then investigated extracellular and cell-associated IL-8 in lipopolysaccharide (LPS)-stimulated BALF cells to determine the IL-8-producing potential of alveolar macrophages (AM). Following LPS stimulation of BALF cells from patients with IPF in the chronic phase, both the extracellular IL-8 in culture fluid and the cell-associated IL-8 in AM were increased as compared with those for the CTL subjects (p< 0.05 and p< 0.05, respectively). These results suggest that AM of patients with IPF are primed for IL-8 production. We conclude that IL-8 may play a role in neutrophilic alveolitis, especially during the subacute phase of IPF.

Original languageEnglish
Pages (from-to)1579-1586
Number of pages8
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume152
Issue number5 I
Publication statusPublished - 1995

Fingerprint

Idiopathic Pulmonary Fibrosis
Alveolar Macrophages
Interleukin-8
Bronchoalveolar Lavage Fluid
Sarcoidosis
Lipopolysaccharides
Cell Culture Techniques

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Priming of alveolar macrophages for interleukin-8 production in patients with idiopathic pulmonary fibrosis. / Nakamura, H.; Fujishima, S.; Waki, Y.; Urano, T.; Sayama, K.; Sakamaki, F.; Terashima, T.; Soejima, K.; Tasaka, S.; Ishizaka, A.; Kawashiro, T.; Kanazawa, M.

In: American Journal of Respiratory and Critical Care Medicine, Vol. 152, No. 5 I, 1995, p. 1579-1586.

Research output: Contribution to journalArticle

Nakamura, H, Fujishima, S, Waki, Y, Urano, T, Sayama, K, Sakamaki, F, Terashima, T, Soejima, K, Tasaka, S, Ishizaka, A, Kawashiro, T & Kanazawa, M 1995, 'Priming of alveolar macrophages for interleukin-8 production in patients with idiopathic pulmonary fibrosis', American Journal of Respiratory and Critical Care Medicine, vol. 152, no. 5 I, pp. 1579-1586.
Nakamura, H. ; Fujishima, S. ; Waki, Y. ; Urano, T. ; Sayama, K. ; Sakamaki, F. ; Terashima, T. ; Soejima, K. ; Tasaka, S. ; Ishizaka, A. ; Kawashiro, T. ; Kanazawa, M. / Priming of alveolar macrophages for interleukin-8 production in patients with idiopathic pulmonary fibrosis. In: American Journal of Respiratory and Critical Care Medicine. 1995 ; Vol. 152, No. 5 I. pp. 1579-1586.
@article{4c31c222844546c784ee985cc8ffac77,
title = "Priming of alveolar macrophages for interleukin-8 production in patients with idiopathic pulmonary fibrosis",
abstract = "We evaluated the contribution of interleukin-8 (IL-8) to the pathogenesis of idiopathic pulmonary fibrosis (IPF) by studying bronchoalveolar lavage fluid (BALF) in eight patients with IPF in the chronically progressive phase, five patients with IPF in the subacutely progressive phase, eight patients with sarcoidosis (SAR), and eight control (CTL) subjects. IL-8 levels were not increased in the BALF of the patients with IPF in the chronic phase (11.3 ± 8.8 pg/ml), nor in that of the SAR patients (13.8 ± 7.8 pg/ml), whereas they were increased in the BALF of patients with IPF in the subacutely progressive phase (1.93 ± 1.10 ng/ml). We then investigated extracellular and cell-associated IL-8 in lipopolysaccharide (LPS)-stimulated BALF cells to determine the IL-8-producing potential of alveolar macrophages (AM). Following LPS stimulation of BALF cells from patients with IPF in the chronic phase, both the extracellular IL-8 in culture fluid and the cell-associated IL-8 in AM were increased as compared with those for the CTL subjects (p< 0.05 and p< 0.05, respectively). These results suggest that AM of patients with IPF are primed for IL-8 production. We conclude that IL-8 may play a role in neutrophilic alveolitis, especially during the subacute phase of IPF.",
author = "H. Nakamura and S. Fujishima and Y. Waki and T. Urano and K. Sayama and F. Sakamaki and T. Terashima and K. Soejima and S. Tasaka and A. Ishizaka and T. Kawashiro and M. Kanazawa",
year = "1995",
language = "English",
volume = "152",
pages = "1579--1586",
journal = "American Journal of Respiratory and Critical Care Medicine",
issn = "1073-449X",
publisher = "American Thoracic Society",
number = "5 I",

}

TY - JOUR

T1 - Priming of alveolar macrophages for interleukin-8 production in patients with idiopathic pulmonary fibrosis

AU - Nakamura, H.

AU - Fujishima, S.

AU - Waki, Y.

AU - Urano, T.

AU - Sayama, K.

AU - Sakamaki, F.

AU - Terashima, T.

AU - Soejima, K.

AU - Tasaka, S.

AU - Ishizaka, A.

AU - Kawashiro, T.

AU - Kanazawa, M.

PY - 1995

Y1 - 1995

N2 - We evaluated the contribution of interleukin-8 (IL-8) to the pathogenesis of idiopathic pulmonary fibrosis (IPF) by studying bronchoalveolar lavage fluid (BALF) in eight patients with IPF in the chronically progressive phase, five patients with IPF in the subacutely progressive phase, eight patients with sarcoidosis (SAR), and eight control (CTL) subjects. IL-8 levels were not increased in the BALF of the patients with IPF in the chronic phase (11.3 ± 8.8 pg/ml), nor in that of the SAR patients (13.8 ± 7.8 pg/ml), whereas they were increased in the BALF of patients with IPF in the subacutely progressive phase (1.93 ± 1.10 ng/ml). We then investigated extracellular and cell-associated IL-8 in lipopolysaccharide (LPS)-stimulated BALF cells to determine the IL-8-producing potential of alveolar macrophages (AM). Following LPS stimulation of BALF cells from patients with IPF in the chronic phase, both the extracellular IL-8 in culture fluid and the cell-associated IL-8 in AM were increased as compared with those for the CTL subjects (p< 0.05 and p< 0.05, respectively). These results suggest that AM of patients with IPF are primed for IL-8 production. We conclude that IL-8 may play a role in neutrophilic alveolitis, especially during the subacute phase of IPF.

AB - We evaluated the contribution of interleukin-8 (IL-8) to the pathogenesis of idiopathic pulmonary fibrosis (IPF) by studying bronchoalveolar lavage fluid (BALF) in eight patients with IPF in the chronically progressive phase, five patients with IPF in the subacutely progressive phase, eight patients with sarcoidosis (SAR), and eight control (CTL) subjects. IL-8 levels were not increased in the BALF of the patients with IPF in the chronic phase (11.3 ± 8.8 pg/ml), nor in that of the SAR patients (13.8 ± 7.8 pg/ml), whereas they were increased in the BALF of patients with IPF in the subacutely progressive phase (1.93 ± 1.10 ng/ml). We then investigated extracellular and cell-associated IL-8 in lipopolysaccharide (LPS)-stimulated BALF cells to determine the IL-8-producing potential of alveolar macrophages (AM). Following LPS stimulation of BALF cells from patients with IPF in the chronic phase, both the extracellular IL-8 in culture fluid and the cell-associated IL-8 in AM were increased as compared with those for the CTL subjects (p< 0.05 and p< 0.05, respectively). These results suggest that AM of patients with IPF are primed for IL-8 production. We conclude that IL-8 may play a role in neutrophilic alveolitis, especially during the subacute phase of IPF.

UR - http://www.scopus.com/inward/record.url?scp=0028844661&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028844661&partnerID=8YFLogxK

M3 - Article

VL - 152

SP - 1579

EP - 1586

JO - American Journal of Respiratory and Critical Care Medicine

JF - American Journal of Respiratory and Critical Care Medicine

SN - 1073-449X

IS - 5 I

ER -