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 Blood, 1 September 2008, Vol. 112, No. 5, pp. 2028-2034.
Prepublished online as a Blood First Edition Paper on June 10, 2008; DOI 10.1182/blood-2008-01-132860.

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PHAGOCYTES

Toll-like receptor–mediated activation of neutrophils by influenza A virus

Jennifer P. Wang1, Glennice N. Bowen1, Carolyn Padden2, Anna Cerny1, Robert W. Finberg1, Peter E. Newburger*,2, and Evelyn A. Kurt-Jones*,1

Departments of1 Medicine and 2 Pediatrics, University of Massachusetts Medical School, Worcester

Influenza virus infection of the respiratory tract is characterized by a neutrophil infiltrate accompanied by inflammatory cytokine and chemokine production. We and others have reported that Toll-like receptor (TLR) proteins are present on human neutrophils and that granulocyte-macrophage colony-stimulating factor (GM-CSF) treatment enhances IL-8 (CXCL8) secretion in response to stimulation with TLR ligands. We demonstrate that influenza virus can induce IL-8 and other inflammatory cytokines from GM-CSF–primed human neutrophils. Using heat inactivation of influenza virus, we show that viral entry but not replication is required for cytokine induction. Furthermore, endosomal acidification and viral uncoating are necessary. Finally, using single-cell analysis of intracellular cytokine accumulation in neutrophils from knockout mice, we prove that TLR7 is essential for influenza viral recognition and inflammatory cytokine production by murine neutrophils. These studies demonstrate neutrophil activation by influenza virus and highlight the importance of TLR7 and TLR8 in that response.


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This article has been cited by other articles:


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Activation of interferon regulatory factor-3 via toll-like receptor 3 and immunomodulatory functions detected in A549 lung epithelial cells exposed to misplaced U1-snRNA
Nucleic Acids Res., June 18, 2009; (2009) gkp525v1.
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