Influenza A virus infection inhibits the efficient recruitment of Th2 cells into the airways and the development of airway eosinophilia

Autor: Gisela Wohlleben, Christine Hambrecht, Heidrun Moll, Ursula Tatsch, Klaus J. Erb, Justus Müller, Edgar Schmitt, Harald Renz, Udo Herz
Rok vydání: 2003
Předmět:
Chemokine
Epitopes
T-Lymphocyte
Immunoglobulin E
medicine.disease_cause
Mice
Cell Movement
Influenza A virus
Immunology and Allergy
Eosinophilia
Chemokine CCL5
Lung
Cells
Cultured
Chemokine CCL2
Mice
Knockout
Mice
Inbred BALB C
biology
medicine.diagnostic_test
respiratory system
Up-Regulation
medicine.anatomical_structure
Chemokines
CC
Goblet Cells
Nippostrongylus
medicine.symptom
Bronchial Hyperreactivity
Chemokine CCL11
Ovalbumin
Immunology
Down-Regulation
Mice
Transgenic
CCL5
Virus
Interferon-gamma
Th2 Cells
Orthomyxoviridae Infections
Lymphopenia
medicine
Animals
Lymphocyte Count
Pulmonary Eosinophilia
Strongylida Infections
Goblet cell
Metaplasia
Allergens
Peptide Fragments
respiratory tract diseases
Mice
Inbred C57BL
Bronchoalveolar lavage
Cell Migration Inhibition
biology.protein
Interleukin-5
Zdroj: Journal of immunology (Baltimore, Md. : 1950). 170(9)
ISSN: 0022-1767
Popis: Most infections with respiratory viruses induce Th1 responses characterized by the generation of Th1 and CD8+ T cells secreting IFN-γ, which in turn have been shown to inhibit the development of Th2 cells. Therefore, it could be expected that respiratory viral infections mediate protection against asthma. However, the opposite seems to be true, because viral infections are often associated with the exacerbation of asthma. For this reason, we investigated what effect an influenza A (flu) virus infection has on the development of asthma. We found that flu infection 1, 3, 6, or 9 wk before allergen airway challenge resulted in a strong suppression of allergen-induced airway eosinophilia. This effect was associated with strongly reduced numbers of Th2 cells in the airways and was not observed in IFN-γ- or IL-12 p35-deficient mice. Mice infected with flu virus and immunized with OVA showed decreased IL-5 and increased IFN-γ, eotaxin/CC chemokine ligand (CCL)11, RANTES/CCL5, and monocyte chemoattractant protein-1/CCL2 levels in the bronchoalveolar lavage fluid, and increased airway hyperreactivity compared with OVA-immunized mice. These results suggest that the flu virus infection reduced airway eosinophilia by inducing Th1 responses, which lead to the inefficient recruitment of Th2 cells into the airways. However, OVA-specific IgE and IgG1 serum levels, blood eosinophilia, and goblet cell metaplasia in the lung were not reduced by the flu infection. Flu virus infection also directly induced AHR and goblet cell metaplasia. Taken together, our results show that flu virus infections can induce, exacerbate, and suppress features of asthmatic disease in mice.
Databáze: OpenAIRE
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