The Increased Expression of HLA-DR and ICAM-1 Molecules by Human Bronchial Epithelial Cells, Induced by Activated Mononuclear Cells, is Downregulated by Nedocromil Sodium
To test the hypothesis that mononuclear cell products could increase the expression of HLA-DR and ICAM-1 molecules in bronchial epithelial cells (BECs), subconfluent cultures of human BECs, obtained from surgically resected bronchi, were incubated with PHA-activated blood mononuclear cell conditione...
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Wiley
1994-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/S0962935194000682 |
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author | O. Sacco S. Lantero L. Scarso V. Frangova V. Ottolini G. A. Rossi |
author_facet | O. Sacco S. Lantero L. Scarso V. Frangova V. Ottolini G. A. Rossi |
author_sort | O. Sacco |
collection | DOAJ |
description | To test the hypothesis that mononuclear cell products could increase
the expression of HLA-DR and ICAM-1 molecules in bronchial
epithelial cells (BECs), subconfluent cultures of human BECs,
obtained from surgically resected bronchi, were incubated with
PHA-activated blood mononuclear cell conditioned media (BCM-CM) or
recombinant IFN-γ. The presence of HLA-DR and ICAM-1 molecules
on BECs was then evaluated by specific antibody staining and
flow-cytometry analysis. The addition to BEC cultures of different
concentrations of PHA-stimulated BMC-CM, or of IFN-γ induced a
dosedependent increase of HIA-DR and ICAM-1 expression, while no
effect was observed with unstimulated BMC-CM. The ability of
nedocromil sodium and, as control, of dexamethasone, to prevent the
upregulation of HLA-DR and ICAM-1 expression on BECs was then
tested. Increasing concentrations (10−7 to 10−4 M) of nedocromil
significandy inhibited HLA-DR and ICAM-1 expression by BECs in a
dose-dependent fashion. A similarly dose-dependent inhibitory effect
was also observed with dexamethasone, which, however, was less
active than nedocromil on HL-ADR expression and more active on
ICAM-1 expression. Finally, nedocromil and dexamethasone showed a
significant synergistic effect on the expression of both cell
surface molecules at the lowest concentrations tested. |
format | Article |
id | doaj-art-999e3d21cca74680a6aa4576ef4431fd |
institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 1994-01-01 |
publisher | Wiley |
record_format | Article |
series | Mediators of Inflammation |
spelling | doaj-art-999e3d21cca74680a6aa4576ef4431fd2025-02-03T01:09:39ZengWileyMediators of Inflammation0962-93511466-18611994-01-0137S7S1310.1155/S0962935194000682The Increased Expression of HLA-DR and ICAM-1 Molecules by Human Bronchial Epithelial Cells, Induced by Activated Mononuclear Cells, is Downregulated by Nedocromil SodiumO. Sacco0S. Lantero1L. Scarso2V. Frangova3V. Ottolini4G. A. Rossi5Divisione di Pneumologia , Istituto G. Gaslini, Largo G. Gaslini 5, Genova 16148, ItalyDivisione di Pneumologia , Istituto G. Gaslini, Largo G. Gaslini 5, Genova 16148, ItalyCentro di Immunoematologia e Servizio Trasfusionale, Istituto G. Gaslini, Largo G. Gaslini 5, Genova 16148, ItalyDivisione di Pneumologia , Istituto G. Gaslini, Largo G. Gaslini 5, Genova 16148, ItalyDivisione di Pneumologia , Istituto G. Gaslini, Largo G. Gaslini 5, Genova 16148, ItalyDivisione di Pneumologia , Istituto G. Gaslini, Largo G. Gaslini 5, Genova 16148, ItalyTo test the hypothesis that mononuclear cell products could increase the expression of HLA-DR and ICAM-1 molecules in bronchial epithelial cells (BECs), subconfluent cultures of human BECs, obtained from surgically resected bronchi, were incubated with PHA-activated blood mononuclear cell conditioned media (BCM-CM) or recombinant IFN-γ. The presence of HLA-DR and ICAM-1 molecules on BECs was then evaluated by specific antibody staining and flow-cytometry analysis. The addition to BEC cultures of different concentrations of PHA-stimulated BMC-CM, or of IFN-γ induced a dosedependent increase of HIA-DR and ICAM-1 expression, while no effect was observed with unstimulated BMC-CM. The ability of nedocromil sodium and, as control, of dexamethasone, to prevent the upregulation of HLA-DR and ICAM-1 expression on BECs was then tested. Increasing concentrations (10−7 to 10−4 M) of nedocromil significandy inhibited HLA-DR and ICAM-1 expression by BECs in a dose-dependent fashion. A similarly dose-dependent inhibitory effect was also observed with dexamethasone, which, however, was less active than nedocromil on HL-ADR expression and more active on ICAM-1 expression. Finally, nedocromil and dexamethasone showed a significant synergistic effect on the expression of both cell surface molecules at the lowest concentrations tested.http://dx.doi.org/10.1155/S0962935194000682 |
spellingShingle | O. Sacco S. Lantero L. Scarso V. Frangova V. Ottolini G. A. Rossi The Increased Expression of HLA-DR and ICAM-1 Molecules by Human Bronchial Epithelial Cells, Induced by Activated Mononuclear Cells, is Downregulated by Nedocromil Sodium Mediators of Inflammation |
title | The Increased Expression of HLA-DR and ICAM-1 Molecules by Human Bronchial Epithelial
Cells, Induced by Activated Mononuclear Cells, is Downregulated by Nedocromil Sodium |
title_full | The Increased Expression of HLA-DR and ICAM-1 Molecules by Human Bronchial Epithelial
Cells, Induced by Activated Mononuclear Cells, is Downregulated by Nedocromil Sodium |
title_fullStr | The Increased Expression of HLA-DR and ICAM-1 Molecules by Human Bronchial Epithelial
Cells, Induced by Activated Mononuclear Cells, is Downregulated by Nedocromil Sodium |
title_full_unstemmed | The Increased Expression of HLA-DR and ICAM-1 Molecules by Human Bronchial Epithelial
Cells, Induced by Activated Mononuclear Cells, is Downregulated by Nedocromil Sodium |
title_short | The Increased Expression of HLA-DR and ICAM-1 Molecules by Human Bronchial Epithelial
Cells, Induced by Activated Mononuclear Cells, is Downregulated by Nedocromil Sodium |
title_sort | increased expression of hla dr and icam 1 molecules by human bronchial epithelial cells induced by activated mononuclear cells is downregulated by nedocromil sodium |
url | http://dx.doi.org/10.1155/S0962935194000682 |
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