A probable role for IFN-gamma in the development of a lung immunopathology in SARS.
Identifieur interne : 004945 ( Main/Exploration ); précédent : 004944; suivant : 004946A probable role for IFN-gamma in the development of a lung immunopathology in SARS.
Auteurs : Michel Theron [Taïwan] ; Kao-Jean Huang ; Yu-Wen Chen ; Ching-Chuan Liu ; Huan-Yao LeiSource :
- Cytokine [ 1043-4666 ] ; 2005.
Descripteurs français
- KwdFr :
- Apoptose (immunologie), Cellules Jurkat, Cellules épithéliales (anatomopathologie), Cellules épithéliales (métabolisme), Communication cellulaire (immunologie), Coronavirus (immunologie), Cycle cellulaire (immunologie), Fibroblastes (anatomopathologie), Fibroblastes (immunologie), Humains, Inhibiteurs de croissance (physiologie), Interféron gamma (physiologie), Lignée cellulaire tumorale, Maladies pulmonaires (anatomopathologie), Maladies pulmonaires (immunologie), Maladies pulmonaires (métabolisme), Prolifération cellulaire, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (métabolisme).
- MESH :
- anatomopathologie : Cellules épithéliales, Fibroblastes, Maladies pulmonaires, Syndrome respiratoire aigu sévère.
- immunologie : Apoptose, Communication cellulaire, Coronavirus, Cycle cellulaire, Fibroblastes, Maladies pulmonaires, Syndrome respiratoire aigu sévère.
- métabolisme : Cellules épithéliales, Maladies pulmonaires, Syndrome respiratoire aigu sévère.
- physiologie : Inhibiteurs de croissance, Interféron gamma.
- Cellules Jurkat, Humains, Lignée cellulaire tumorale, Prolifération cellulaire.
English descriptors
- KwdEn :
- Apoptosis (immunology), Cell Communication (immunology), Cell Cycle (immunology), Cell Line, Tumor, Cell Proliferation, Coronavirus (immunology), Epithelial Cells (metabolism), Epithelial Cells (pathology), Fibroblasts (immunology), Fibroblasts (pathology), Growth Inhibitors (physiology), Humans, Interferon-gamma (physiology), Jurkat Cells, Lung Diseases (immunology), Lung Diseases (metabolism), Lung Diseases (pathology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (pathology), fas Receptor (biosynthesis), fas Receptor (genetics), fas Receptor (immunology).
- MESH :
- chemical , biosynthesis : fas Receptor.
- chemical , genetics : fas Receptor.
- chemical , immunology : fas Receptor.
- chemical , physiology : Growth Inhibitors, Interferon-gamma.
- immunology : Apoptosis, Cell Communication, Cell Cycle, Coronavirus, Fibroblasts, Lung Diseases, Severe Acute Respiratory Syndrome.
- metabolism : Epithelial Cells, Lung Diseases, Severe Acute Respiratory Syndrome.
- pathology : Epithelial Cells, Fibroblasts, Lung Diseases, Severe Acute Respiratory Syndrome.
- Cell Line, Tumor, Cell Proliferation, Humans, Jurkat Cells.
Abstract
Recent work carried out in our laboratory showed the existence of a cytokine storm in SARS patients, dominated by Th1-type mediators. We thus hypothesized that IFN-gamma may play a major role in the pathology by triggering immune-mediated alveolar damage. As we assessed or re-assessed some effects of IFN-gamma on a number of human lung epithelial and fibroblast cell lines, chosen for their wide use in the literature, we found that alveolar epithelial cells were more sensitive to IFN-gamma, in terms of proliferation inhibition and enhancement of Fas-mediated apoptosis. While similar effects were obtained on fibroblasts, concentrations of IFN-gamma 4--8-fold greater were required. In addition, both epithelial and fibroblastic cell lines were able to secrete large quantities of T cell-targeting chemokines, similar to the ones detected in SARS patients. Based on the clinical data collected previously, the available literature and our in vitro experimentation, we propose that IFN-gamma may be responsible for acute lung injury in the late phase of the SARS pathology.
DOI: 10.1016/j.cyto.2005.07.007
PubMed: 16129616
Affiliations:
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Le document en format XML
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We thus hypothesized that IFN-gamma may play a major role in the pathology by triggering immune-mediated alveolar damage. As we assessed or re-assessed some effects of IFN-gamma on a number of human lung epithelial and fibroblast cell lines, chosen for their wide use in the literature, we found that alveolar epithelial cells were more sensitive to IFN-gamma, in terms of proliferation inhibition and enhancement of Fas-mediated apoptosis. While similar effects were obtained on fibroblasts, concentrations of IFN-gamma 4--8-fold greater were required. In addition, both epithelial and fibroblastic cell lines were able to secrete large quantities of T cell-targeting chemokines, similar to the ones detected in SARS patients. Based on the clinical data collected previously, the available literature and our in vitro experimentation, we propose that IFN-gamma may be responsible for acute lung injury in the late phase of the SARS pathology.</div></front></TEI><affiliations><list><country><li>Taïwan</li></country></list><tree><noCountry><name sortKey="Chen, Yu Wen" sort="Chen, Yu Wen" uniqKey="Chen Y" first="Yu-Wen" last="Chen">Yu-Wen Chen</name><name sortKey="Huang, Kao Jean" sort="Huang, Kao Jean" uniqKey="Huang K" first="Kao-Jean" last="Huang">Kao-Jean Huang</name><name sortKey="Lei, Huan Yao" sort="Lei, Huan Yao" uniqKey="Lei H" first="Huan-Yao" last="Lei">Huan-Yao Lei</name><name sortKey="Liu, Ching Chuan" sort="Liu, Ching Chuan" uniqKey="Liu C" first="Ching-Chuan" last="Liu">Ching-Chuan Liu</name></noCountry><country name="Taïwan"><noRegion><name sortKey="Theron, Michel" sort="Theron, Michel" uniqKey="Theron M" first="Michel" last="Theron">Michel Theron</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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