Interleukin-1β and interferon-γ differentially regulate release of monocyte chemotactic protein-1 and interleukin-8 by human bronchial epithelial cells

Vincent H J Van Der Velden, Mascha M. Verheggen, Sergio Bernasconi, Silvano Sozzani, Brigitta A E Naber, Carin A J Van Der Linden-van Beurden, Henk C. Hoogsteden, Alberto Mantovani, Marjan Versnel

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Airway inflammation is characterized by an accumulation of activated leukocytes. Bronchial epithelial cells may contribute to this process by releasing chemokines and by expressing surface membrane molecules involved in the adhesion and activation of the recruited leukocytes. In this study, we analyzed the effects of cytokines and glucocorticoids on the release of monocyte chemotactic protein-1 (MCP-1), a potent chemoattractant for predominantly monocytes and lymphocytes, by human bronchial epithelial cells and compared this with the release of interleukin-8 (IL-8), which potently attracts neutrophils. In addition, we analyzed the effects of cytokines and glucocorticoids on the epithelial expression of intercellular adhesion molecule (ICAM)-1, CD40, and human leukocyte antigen (HLA) class II molecules. Primary cultures of human bronchial epithelial cells constitutively released MCP-1 and IL-8. IFN-γ greatly increased MCP-1 release, which was accompanied by increased expression of MCP-1 mRNA and an increased monocyte chemotactic potential. In contrast, IFN-γ had no effect on the release of IL-8, but it did increase the epithelial expression of ICAM-1, CD40, and HLA class II molecules. IL-1β increased both MCP-1 and IL-8 release, and increased the expression of ICAM-1 and CD40, but not HLA class II molecules. Dexamethasone partially inhibited the cytokine-induced release of MCP-1 and IL-8 and the expression of ICAM-1, CD40, and HLA class II molecules by human bronchial epithelial cells. Our results indicate that IFN-γ and IL-1β differentially regulate the MCP-1 and IL-8 release by human bronchial epithelial cells. In addition, IL-1β and particularly IFN-γ increase the expression of ICAM-1, HLA class II and/or CD40 molecules, which are involved in the adhesion and possibly activation of the recruited leukocytes. Finally, the beneficial effect of glucocorticoid therapy in airway inflammatory diseases may be mediated in part by inhibition of chemokine release and ICAM-1, CD40, and HLA class II expression by bronchial epithelial cells.

Original languageEnglish
Pages (from-to)269-277
Number of pages9
JournalEuropean Cytokine Network
Volume9
Issue number3
Publication statusPublished - 1998

Fingerprint

Chemokine CCL2
Interleukin-8
Interleukin-1
Interferons
Intercellular Adhesion Molecule-1
HLA Antigens
Epithelial Cells
Molecules
Glucocorticoids
Leukocytes
Cytokines
Chemokines
Monocytes
Adhesion
Chemical activation
Lymphocytes
Chemotactic Factors
Dexamethasone
Neutrophils
Inflammation

Keywords

  • Bronchial epithelial cells
  • Cytokines
  • Glucocorticoids
  • IL-8
  • MCP-1

ASJC Scopus subject areas

  • Immunology
  • Cell Biology

Cite this

Van Der Velden, V. H. J., Verheggen, M. M., Bernasconi, S., Sozzani, S., Naber, B. A. E., Van Der Linden-van Beurden, C. A. J., ... Versnel, M. (1998). Interleukin-1β and interferon-γ differentially regulate release of monocyte chemotactic protein-1 and interleukin-8 by human bronchial epithelial cells. European Cytokine Network, 9(3), 269-277.

Interleukin-1β and interferon-γ differentially regulate release of monocyte chemotactic protein-1 and interleukin-8 by human bronchial epithelial cells. / Van Der Velden, Vincent H J; Verheggen, Mascha M.; Bernasconi, Sergio; Sozzani, Silvano; Naber, Brigitta A E; Van Der Linden-van Beurden, Carin A J; Hoogsteden, Henk C.; Mantovani, Alberto; Versnel, Marjan.

In: European Cytokine Network, Vol. 9, No. 3, 1998, p. 269-277.

Research output: Contribution to journalArticle

Van Der Velden, VHJ, Verheggen, MM, Bernasconi, S, Sozzani, S, Naber, BAE, Van Der Linden-van Beurden, CAJ, Hoogsteden, HC, Mantovani, A & Versnel, M 1998, 'Interleukin-1β and interferon-γ differentially regulate release of monocyte chemotactic protein-1 and interleukin-8 by human bronchial epithelial cells', European Cytokine Network, vol. 9, no. 3, pp. 269-277.
Van Der Velden, Vincent H J ; Verheggen, Mascha M. ; Bernasconi, Sergio ; Sozzani, Silvano ; Naber, Brigitta A E ; Van Der Linden-van Beurden, Carin A J ; Hoogsteden, Henk C. ; Mantovani, Alberto ; Versnel, Marjan. / Interleukin-1β and interferon-γ differentially regulate release of monocyte chemotactic protein-1 and interleukin-8 by human bronchial epithelial cells. In: European Cytokine Network. 1998 ; Vol. 9, No. 3. pp. 269-277.
@article{38aed003ff22451ab68bfac5a1fb88a7,
title = "Interleukin-1β and interferon-γ differentially regulate release of monocyte chemotactic protein-1 and interleukin-8 by human bronchial epithelial cells",
abstract = "Airway inflammation is characterized by an accumulation of activated leukocytes. Bronchial epithelial cells may contribute to this process by releasing chemokines and by expressing surface membrane molecules involved in the adhesion and activation of the recruited leukocytes. In this study, we analyzed the effects of cytokines and glucocorticoids on the release of monocyte chemotactic protein-1 (MCP-1), a potent chemoattractant for predominantly monocytes and lymphocytes, by human bronchial epithelial cells and compared this with the release of interleukin-8 (IL-8), which potently attracts neutrophils. In addition, we analyzed the effects of cytokines and glucocorticoids on the epithelial expression of intercellular adhesion molecule (ICAM)-1, CD40, and human leukocyte antigen (HLA) class II molecules. Primary cultures of human bronchial epithelial cells constitutively released MCP-1 and IL-8. IFN-γ greatly increased MCP-1 release, which was accompanied by increased expression of MCP-1 mRNA and an increased monocyte chemotactic potential. In contrast, IFN-γ had no effect on the release of IL-8, but it did increase the epithelial expression of ICAM-1, CD40, and HLA class II molecules. IL-1β increased both MCP-1 and IL-8 release, and increased the expression of ICAM-1 and CD40, but not HLA class II molecules. Dexamethasone partially inhibited the cytokine-induced release of MCP-1 and IL-8 and the expression of ICAM-1, CD40, and HLA class II molecules by human bronchial epithelial cells. Our results indicate that IFN-γ and IL-1β differentially regulate the MCP-1 and IL-8 release by human bronchial epithelial cells. In addition, IL-1β and particularly IFN-γ increase the expression of ICAM-1, HLA class II and/or CD40 molecules, which are involved in the adhesion and possibly activation of the recruited leukocytes. Finally, the beneficial effect of glucocorticoid therapy in airway inflammatory diseases may be mediated in part by inhibition of chemokine release and ICAM-1, CD40, and HLA class II expression by bronchial epithelial cells.",
keywords = "Bronchial epithelial cells, Cytokines, Glucocorticoids, IL-8, MCP-1",
author = "{Van Der Velden}, {Vincent H J} and Verheggen, {Mascha M.} and Sergio Bernasconi and Silvano Sozzani and Naber, {Brigitta A E} and {Van Der Linden-van Beurden}, {Carin A J} and Hoogsteden, {Henk C.} and Alberto Mantovani and Marjan Versnel",
year = "1998",
language = "English",
volume = "9",
pages = "269--277",
journal = "Environmental and Molecular Mutagenesis",
issn = "0893-6692",
publisher = "John Libbey Eurotext",
number = "3",

}

TY - JOUR

T1 - Interleukin-1β and interferon-γ differentially regulate release of monocyte chemotactic protein-1 and interleukin-8 by human bronchial epithelial cells

AU - Van Der Velden, Vincent H J

AU - Verheggen, Mascha M.

AU - Bernasconi, Sergio

AU - Sozzani, Silvano

AU - Naber, Brigitta A E

AU - Van Der Linden-van Beurden, Carin A J

AU - Hoogsteden, Henk C.

AU - Mantovani, Alberto

AU - Versnel, Marjan

PY - 1998

Y1 - 1998

N2 - Airway inflammation is characterized by an accumulation of activated leukocytes. Bronchial epithelial cells may contribute to this process by releasing chemokines and by expressing surface membrane molecules involved in the adhesion and activation of the recruited leukocytes. In this study, we analyzed the effects of cytokines and glucocorticoids on the release of monocyte chemotactic protein-1 (MCP-1), a potent chemoattractant for predominantly monocytes and lymphocytes, by human bronchial epithelial cells and compared this with the release of interleukin-8 (IL-8), which potently attracts neutrophils. In addition, we analyzed the effects of cytokines and glucocorticoids on the epithelial expression of intercellular adhesion molecule (ICAM)-1, CD40, and human leukocyte antigen (HLA) class II molecules. Primary cultures of human bronchial epithelial cells constitutively released MCP-1 and IL-8. IFN-γ greatly increased MCP-1 release, which was accompanied by increased expression of MCP-1 mRNA and an increased monocyte chemotactic potential. In contrast, IFN-γ had no effect on the release of IL-8, but it did increase the epithelial expression of ICAM-1, CD40, and HLA class II molecules. IL-1β increased both MCP-1 and IL-8 release, and increased the expression of ICAM-1 and CD40, but not HLA class II molecules. Dexamethasone partially inhibited the cytokine-induced release of MCP-1 and IL-8 and the expression of ICAM-1, CD40, and HLA class II molecules by human bronchial epithelial cells. Our results indicate that IFN-γ and IL-1β differentially regulate the MCP-1 and IL-8 release by human bronchial epithelial cells. In addition, IL-1β and particularly IFN-γ increase the expression of ICAM-1, HLA class II and/or CD40 molecules, which are involved in the adhesion and possibly activation of the recruited leukocytes. Finally, the beneficial effect of glucocorticoid therapy in airway inflammatory diseases may be mediated in part by inhibition of chemokine release and ICAM-1, CD40, and HLA class II expression by bronchial epithelial cells.

AB - Airway inflammation is characterized by an accumulation of activated leukocytes. Bronchial epithelial cells may contribute to this process by releasing chemokines and by expressing surface membrane molecules involved in the adhesion and activation of the recruited leukocytes. In this study, we analyzed the effects of cytokines and glucocorticoids on the release of monocyte chemotactic protein-1 (MCP-1), a potent chemoattractant for predominantly monocytes and lymphocytes, by human bronchial epithelial cells and compared this with the release of interleukin-8 (IL-8), which potently attracts neutrophils. In addition, we analyzed the effects of cytokines and glucocorticoids on the epithelial expression of intercellular adhesion molecule (ICAM)-1, CD40, and human leukocyte antigen (HLA) class II molecules. Primary cultures of human bronchial epithelial cells constitutively released MCP-1 and IL-8. IFN-γ greatly increased MCP-1 release, which was accompanied by increased expression of MCP-1 mRNA and an increased monocyte chemotactic potential. In contrast, IFN-γ had no effect on the release of IL-8, but it did increase the epithelial expression of ICAM-1, CD40, and HLA class II molecules. IL-1β increased both MCP-1 and IL-8 release, and increased the expression of ICAM-1 and CD40, but not HLA class II molecules. Dexamethasone partially inhibited the cytokine-induced release of MCP-1 and IL-8 and the expression of ICAM-1, CD40, and HLA class II molecules by human bronchial epithelial cells. Our results indicate that IFN-γ and IL-1β differentially regulate the MCP-1 and IL-8 release by human bronchial epithelial cells. In addition, IL-1β and particularly IFN-γ increase the expression of ICAM-1, HLA class II and/or CD40 molecules, which are involved in the adhesion and possibly activation of the recruited leukocytes. Finally, the beneficial effect of glucocorticoid therapy in airway inflammatory diseases may be mediated in part by inhibition of chemokine release and ICAM-1, CD40, and HLA class II expression by bronchial epithelial cells.

KW - Bronchial epithelial cells

KW - Cytokines

KW - Glucocorticoids

KW - IL-8

KW - MCP-1

UR - http://www.scopus.com/inward/record.url?scp=0031593387&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031593387&partnerID=8YFLogxK

M3 - Article

C2 - 9831176

AN - SCOPUS:0031593387

VL - 9

SP - 269

EP - 277

JO - Environmental and Molecular Mutagenesis

JF - Environmental and Molecular Mutagenesis

SN - 0893-6692

IS - 3

ER -