Eosinophils contribute to innate antiviral immunity and promote clearance of respiratory syncytial virus

Phipps, Simon, Lam, Chuan En, Mahalingam, Suresh, Newhouse, Matthew, Ramirez, Ruben, Rosenberg, Helene F., Foster, Paul S. and Matthaei, Klaus I. (2007) Eosinophils contribute to innate antiviral immunity and promote clearance of respiratory syncytial virus. Blood, 110 5: 1578-1586. doi:10.1182/blood-2007-01-071340


Author Phipps, Simon
Lam, Chuan En
Mahalingam, Suresh
Newhouse, Matthew
Ramirez, Ruben
Rosenberg, Helene F.
Foster, Paul S.
Matthaei, Klaus I.
Title Eosinophils contribute to innate antiviral immunity and promote clearance of respiratory syncytial virus
Journal name Blood   Check publisher's open access policy
ISSN 0006-4971
1528-0020
Publication date 2007-09-01
Year available 2007
Sub-type Article (original research)
DOI 10.1182/blood-2007-01-071340
Open Access Status Not yet assessed
Volume 110
Issue 5
Start page 1578
End page 1586
Total pages 9
Place of publication Washington, DC, United States
Publisher American Society of Hematology
Language eng
Subject 1303 Biochemistry
2403 Immunology
2720 Hematology
1307 Cell Biology
Abstract 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.
Keyword Hematology
Hematology
HEMATOLOGY
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Biomedical Sciences Publications
 
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Created: Thu, 10 Mar 2011, 00:31:40 EST