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Details

Autor(en) / Beteiligte
Titel
Eosinophils contribute to innate antiviral immunity and promote clearance of respiratory syncytial virus
Ist Teil von
  • Blood, 2007-09, Vol.110 (5), p.1578-1586
Ort / Verlag
United States: Elsevier Inc
Erscheinungsjahr
2007
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
  • Eosinophils are recruited to the lungs in response to respiratory syncytial virus (RSV) infection; however, their role in promoting antiviral host defense remains unclear. Here, we demonstrate that eosinophils express TLRs that recognize viral nucleic acids, are activated and degranulate after single-stranded RNA (ssRNA) stimulation of the TLR-7–MyD88 pathway, and provide host defense against RSV that is MyD88 dependent. In contrast to wild-type mice, virus clearance from lung tissue was more rapid in hypereosinophilic (interleukin-5 transgenic) mice. Transfer of wild-type but not MyD88-deficient eosinophils to the lungs of RSV-infected wild-type mice accelerated virus clearance and inhibited the development of airways hyperreactivity. Similar responses were observed when infected recipient mice were MyD88 deficient. Eosinophils isolated from infected hypereosinophilic MyD88-sufficient but not MyD88-deficient mice expressed greater amounts of IFN regulatory factor (IRF)–7 and eosinophil-associated ribonucleases EAR-1 and EAR-2. Hypereosinophilia in the airways of infected mice also correlated with increased expression of IRF-7, IFN-β, and NOS-2, and inhibition of NO production with the NOS-2 inhibitor L-NMA partially reversed the accelerated virus clearance promoted by eosinophils. Collectively, our results demonstrate that eosinophils can protect against RSV in vivo, as they promote virus clearance and may thus limit virus-induced lung dysfunction.
Sprache
Englisch
Identifikatoren
ISSN: 0006-4971
eISSN: 1528-0020
DOI: 10.1182/blood-2007-01-071340
Titel-ID: cdi_crossref_primary_10_1182_blood_2007_01_071340
Format
Schlagworte
Animals, Enzyme Inhibitors - pharmacology, Eosinophil-Derived Neurotoxin - biosynthesis, Eosinophil-Derived Neurotoxin - immunology, Eosinophils - immunology, Eosinophils - metabolism, Eosinophils - ultrastructure, Immunity, Innate, Interferon Regulatory Factor-7 - biosynthesis, Interferon Regulatory Factor-7 - immunology, Interferon-beta - biosynthesis, Interferon-beta - immunology, Interleukin-5 - biosynthesis, Interleukin-5 - immunology, Lung - immunology, Lung - metabolism, Lung - ultrastructure, Lung - virology, Membrane Glycoproteins - immunology, Membrane Glycoproteins - metabolism, Mice, Mice, Inbred BALB C, Mice, Transgenic, Myeloid Differentiation Factor 88 - deficiency, Myeloid Differentiation Factor 88 - immunology, Nitric Oxide - immunology, Nitric Oxide - metabolism, Nitric Oxide Synthase Type II - antagonists & inhibitors, Nitric Oxide Synthase Type II - biosynthesis, Nitric Oxide Synthase Type II - immunology, Respiratory Hypersensitivity - genetics, Respiratory Hypersensitivity - immunology, Respiratory Hypersensitivity - metabolism, Respiratory Hypersensitivity - pathology, Respiratory Syncytial Virus Infections - genetics, Respiratory Syncytial Virus Infections - immunology, Respiratory Syncytial Virus Infections - metabolism, Respiratory Syncytial Virus Infections - pathology, Respiratory Syncytial Viruses - immunology, RNA, Viral - immunology, RNA, Viral - metabolism, Signal Transduction - drug effects, Signal Transduction - immunology, Toll-Like Receptor 7 - immunology, Toll-Like Receptor 7 - metabolism

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