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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Kanda, Akira Driss, Virginie Hornez, Nicolas Abdallah, Marwan Roumier, Thomas Abboud, Georges Legrand, Fanny Staumont-Sallé, Delphine Quéant, Severine Bertout, Julie Fleury, Sébastien Rémy, Patrick Papin, Jean-Paul Julia, Valérie Capron, Monique Dombrowicz, David |
| Description | Country affiliation: France Author Affiliation: Kanda A ( Inserm U547, Lille, France) |
| Abstract | BACKGROUND: Eosinophils are key players in T(H)2-driven pathologies, such as allergic lung inflammation. After IL-5- and eotaxin-mediated tissue recruitment, they release several cytotoxic and inflammatory mediators. However, their exact contribution to asthma remains controversial. Indeed, in human subjects anti-IL-5 treatment inhibits eosinophilia but not antigen-induced airway hyperresponsiveness (AHR). Likewise, lung fibrosis is abrogated in 2 strains of eosinophil-deficient mice, whereas AHR is inhibited in only one of them. Finally, eosinophils have been shown to attract T(H)2 lymphocytes at the inflammatory site. OBJECTIVE: The ability of eosinophils to promote AHR and lung inflammation independently of lymphocytes was investigated. METHODS: Adoptive transfers of resting or activated eosinophils from IL-5 transgenic mice were performed into naive BALB/c mice, mice with severe combined immunodeficiency, and IFN-gamma-deficient BALB/c recipients. RESULTS: Adoptively transferred eosinophils induced lung inflammation, fibrosis, collagen deposition, and AHR not only in BALB/c mice but also in recipient mice with severe combined immunodeficiency. Surprisingly, IFN-gamma expression was increased in lungs from eosinophil-transferred animals. Furthermore, IFN-gamma neutralization in recipients partially inhibited eosinophil-induced AHR. Moreover, IFN-gamma-deficient eosinophils or eosinophils treated with a blocking anti-IFN-gamma receptor antibody failed to induce AHR in IFN-gamma-deficient recipients. Finally, in vitro and at low concentrations, IFN-gamma increased eosinophil peroxidase release, potentiated chemotaxis, and prolonged survival, suggesting the existence of an autocrine mechanism. CONCLUSIONS: These results support the important and previously unsuspected contribution of eosinophils to lung inflammation independently of lymphocytes through production of IFN-gamma, the prototypical T(H)1 cytokine. |
| File Format | HTM / HTML |
| ISSN | 00916749 |
| e-ISSN | 10976825 |
| Journal | Journal of Allergy and Clinical Immunology |
| Issue Number | 3 |
| Volume Number | 124 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2009-09-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Discipline Immunology Bronchial Hyperreactivity Immunology Eosinophils Interferon-gamma Metabolism Interleukin-5 Lymphocytes Pneumonia Adoptive Transfer Animals Etiology Chemotaxis Eosinophil Peroxidase Genetics Lung Pathology Mice Mice, Inbred Balb C Mice, Knockout Mice, Scid Mice, Transgenic Receptors, Interferon Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Immunology and Allergy Immunology |
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