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 language | English |
|---|---|
| Pages (from-to) | 269-277 |
| Number of pages | 9 |
| Journal | European Cytokine Network |
| Volume | 9 |
| Issue number | 3 |
| Publication status | Published - 1998 |
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Keywords
- Bronchial epithelial cells
- Cytokines
- Glucocorticoids
- IL-8
- MCP-1
ASJC Scopus subject areas
- Immunology
- Cell Biology
Cite this
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 journal › Article
}
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 -