Bronchial epithelial cells of patients with asthma release chemoattractant factors for T lymphocytes

Background: T lymphocytes may orchestrate the inflammatory response in atopic asthma, but the mechanisms that promote T-cell accumulation in asthmatic airways are still unclear. In this study, we tested the hypothesis that bronchial epithelial cells of patients with atopic asthma release chemoattrac...

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Published inJournal of allergy and clinical immunology Vol. 92; no. 3; pp. 412 - 424
Main Authors Bellini, Alberto, Yoshimura, Hiroshi, Vittori, Enza, Marini, Maurizio, Mattoli, Sabrina
Format Journal Article
LanguageEnglish
Published New York, NY Mosby, Inc 01.09.1993
Elsevier
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Abstract Background: T lymphocytes may orchestrate the inflammatory response in atopic asthma, but the mechanisms that promote T-cell accumulation in asthmatic airways are still unclear. In this study, we tested the hypothesis that bronchial epithelial cells of patients with atopic asthma release chemoattractant factors for T lymphocytes. Methods: Sixteen patients with atopic asthma and eight healthy control subjects were selected for this study. Bronchial epithelial cells were isolated from biopsy specimens obtained by means of bronchoscopy and cultured for 48 hours in serum- and hormone-free medium, with or without 10 −6 mol/L histamine. Results: Only the supernatants of cells from donors with asthma showed chemotactic activity for T lymphocytes, and this was significantly increased ( p < 0.025) by exposure to histamine. Chemotactic activity was in part mediated by interkukin-8 (IL-8), because an antibody against human IL-8 significantly reduced it ( p < 0.05) and the cell supematants contained appreciable amounts of immunoreactive IL-8 (0.89 ± 0.39 ng/ml). Both the residual chemotactic activity of unstimulated epithelial cells and the increased activity caused by histamine were mediated by a single protease-sensitive substance with an apparent molecular weight of 56,000 d and an extimated isoelectric point of 8.8 to 9.1. The partially purified chemoattractant specifically enhanced the migration of CD4+ T lymphocytes, and its activity was inhibited by the univalent Fab fragment of a monoclonal antibody against CD4. Conclusion: These results extend our previous observations, indicating an important effector role of bronchial epithelium in asthma.
AbstractList T lymphocytes may orchestrate the inflammatory response in atopic asthma, but the mechanisms that promote T-cell accumulation in asthmatic airways are still unclear. In this study, we tested the hypothesis that bronchial epithelial cells of patients with atopic asthma release chemoattractant factors for T lymphocytes. Sixteen patients with atopic asthma and eight healthy control subjects were selected for this study. Bronchial epithelial cells were isolated from biopsy specimens obtained by means of bronchoscopy and cultured for 48 hours in serum- and hormone-free medium, with or without 10(-6) mol/L histamine. Only the supernatants of cells from donors with asthma showed chemotactic activity for T lymphocytes, and this was significantly increased (p < 0.025) by exposure to histamine. Chemotactic activity was in part mediated by interleukin-8 (IL-8), because an antibody against human IL-8 significantly reduced it (p < 0.05) and the cell supernatants contained appreciable amounts of immunoreactive IL-8 (0.89 +/- 0.39 ng/ml). Both the residual chemotactic activity of unstimulated epithelial cells and the increased activity caused by histamine were mediated by a single protease-sensitive substance with an apparent molecular weight of 56,000 d and an estimated isoelectric point of 8.8 to 9.1. The partially purified chemoattractant specifically enhanced the migration of CD4+ T lymphocytes, and its activity was inhibited by the univalent Fab fragment of a monoclonal antibody against CD4. These results extend our previous observations, indicating an important effector role of bronchial epithelium in asthma.
Background: T lymphocytes may orchestrate the inflammatory response in atopic asthma, but the mechanisms that promote T-cell accumulation in asthmatic airways are still unclear. In this study, we tested the hypothesis that bronchial epithelial cells of patients with atopic asthma release chemoattractant factors for T lymphocytes. Methods: Sixteen patients with atopic asthma and eight healthy control subjects were selected for this study. Bronchial epithelial cells were isolated from biopsy specimens obtained by means of bronchoscopy and cultured for 48 hours in serum- and hormone-free medium, with or without 10 −6 mol/L histamine. Results: Only the supernatants of cells from donors with asthma showed chemotactic activity for T lymphocytes, and this was significantly increased ( p < 0.025) by exposure to histamine. Chemotactic activity was in part mediated by interkukin-8 (IL-8), because an antibody against human IL-8 significantly reduced it ( p < 0.05) and the cell supematants contained appreciable amounts of immunoreactive IL-8 (0.89 ± 0.39 ng/ml). Both the residual chemotactic activity of unstimulated epithelial cells and the increased activity caused by histamine were mediated by a single protease-sensitive substance with an apparent molecular weight of 56,000 d and an extimated isoelectric point of 8.8 to 9.1. The partially purified chemoattractant specifically enhanced the migration of CD4+ T lymphocytes, and its activity was inhibited by the univalent Fab fragment of a monoclonal antibody against CD4. Conclusion: These results extend our previous observations, indicating an important effector role of bronchial epithelium in asthma.
T lymphocytes may orchestrate the inflammatory response in atopic asthma, but the mechanisms that promote T-cell accumulation in asthmatic airways are still unclear. In this study, we tested the hypothesis that bronchial epithelial cells of patients with atopic asthma release chemoattractant factors for T lymphocytes.BACKGROUNDT lymphocytes may orchestrate the inflammatory response in atopic asthma, but the mechanisms that promote T-cell accumulation in asthmatic airways are still unclear. In this study, we tested the hypothesis that bronchial epithelial cells of patients with atopic asthma release chemoattractant factors for T lymphocytes.Sixteen patients with atopic asthma and eight healthy control subjects were selected for this study. Bronchial epithelial cells were isolated from biopsy specimens obtained by means of bronchoscopy and cultured for 48 hours in serum- and hormone-free medium, with or without 10(-6) mol/L histamine.METHODSSixteen patients with atopic asthma and eight healthy control subjects were selected for this study. Bronchial epithelial cells were isolated from biopsy specimens obtained by means of bronchoscopy and cultured for 48 hours in serum- and hormone-free medium, with or without 10(-6) mol/L histamine.Only the supernatants of cells from donors with asthma showed chemotactic activity for T lymphocytes, and this was significantly increased (p < 0.025) by exposure to histamine. Chemotactic activity was in part mediated by interleukin-8 (IL-8), because an antibody against human IL-8 significantly reduced it (p < 0.05) and the cell supernatants contained appreciable amounts of immunoreactive IL-8 (0.89 +/- 0.39 ng/ml). Both the residual chemotactic activity of unstimulated epithelial cells and the increased activity caused by histamine were mediated by a single protease-sensitive substance with an apparent molecular weight of 56,000 d and an estimated isoelectric point of 8.8 to 9.1. The partially purified chemoattractant specifically enhanced the migration of CD4+ T lymphocytes, and its activity was inhibited by the univalent Fab fragment of a monoclonal antibody against CD4.RESULTSOnly the supernatants of cells from donors with asthma showed chemotactic activity for T lymphocytes, and this was significantly increased (p < 0.025) by exposure to histamine. Chemotactic activity was in part mediated by interleukin-8 (IL-8), because an antibody against human IL-8 significantly reduced it (p < 0.05) and the cell supernatants contained appreciable amounts of immunoreactive IL-8 (0.89 +/- 0.39 ng/ml). Both the residual chemotactic activity of unstimulated epithelial cells and the increased activity caused by histamine were mediated by a single protease-sensitive substance with an apparent molecular weight of 56,000 d and an estimated isoelectric point of 8.8 to 9.1. The partially purified chemoattractant specifically enhanced the migration of CD4+ T lymphocytes, and its activity was inhibited by the univalent Fab fragment of a monoclonal antibody against CD4.These results extend our previous observations, indicating an important effector role of bronchial epithelium in asthma.CONCLUSIONThese results extend our previous observations, indicating an important effector role of bronchial epithelium in asthma.
T lymphocytes may orchestrate the inflammatory response in atopic asthma, but the mechanisms that promote T-cell accumulation in asthmatic airways are still unclear. In this study, we tested the hypothesis that bronchial epithelial cells of patients with atopic asthma release chemoattractant factors for T lymphocytes. Sixteen patients with atopic asthma and eight healthy control subjects were selected for this study. Bronchial epithelial cells were isolated from biopsy specimens obtained by means of bronchoscopy and cultured for 48 hours in serum- and hormone-free medium, with or without 10 super(-6) mol/L histamine. The results extend our previous observations, indicating an important effector role of bronchial epithelium in asthma.
Author Bellini, Alberto
Marini, Maurizio
Yoshimura, Hiroshi
Mattoli, Sabrina
Vittori, Enza
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Issue 3
Keywords T lymphocytes
interkukin-8
PBS
EC-CM
FEV 1
IL
EC-CF
asthma
PC20M
Airway epithelium
lymphocyte chemoattractant factor
LCF
Human
Allergy
Immunopathology
Respiratory disease
T-Lymphocyte
Bronchus
Exploration
Epithelium
Chemotactic factor
Asthma
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Snippet Background: T lymphocytes may orchestrate the inflammatory response in atopic asthma, but the mechanisms that promote T-cell accumulation in asthmatic airways...
T lymphocytes may orchestrate the inflammatory response in atopic asthma, but the mechanisms that promote T-cell accumulation in asthmatic airways are still...
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SubjectTerms Adult
Airway epithelium
Allergic diseases
asthma
Asthma - immunology
Biological and medical sciences
Bronchi - immunology
Bronchi - pathology
Cells, Cultured
Chemotactic Factors - biosynthesis
Chemotaxis, Leukocyte - drug effects
Chemotaxis, Leukocyte - immunology
Epithelium - immunology
Epithelium - pathology
Female
Histamine - pharmacology
Humans
Immunopathology
interkukin-8
Interleukin-8 - biosynthesis
lymphocyte chemoattractant factor
Male
Medical sciences
Respiratory and ent allergic diseases
T lymphocytes
T-Lymphocytes - immunology
Title Bronchial epithelial cells of patients with asthma release chemoattractant factors for T lymphocytes
URI https://dx.doi.org/10.1016/0091-6749(93)90120-5
https://www.ncbi.nlm.nih.gov/pubmed/8360392
https://www.proquest.com/docview/16806705
https://www.proquest.com/docview/75923558
Volume 92
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