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DAMP Molecule S100A9 Acts as a Molecular Pattern to Enhance Inflammation during Influenza A Virus Infection: Role of DDX21-TRIF-TLR4-MyD88 Pathway
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DAMP Molecule S100A9 Acts as a Molecular Pattern to Enhance Inflammation during Influenza A Virus Infection: Role of DDX21-TRIF-TLR4-MyD88 Pathway
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DAMP Molecule S100A9 Acts as a Molecular Pattern to Enhance Inflammation during Influenza A Virus Infection: Role of DDX21-TRIF-TLR4-MyD88 Pathway
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Journal Article
DAMP Molecule S100A9 Acts as a Molecular Pattern to Enhance Inflammation during Influenza A Virus Infection: Role of DDX21-TRIF-TLR4-MyD88 Pathway
2014
Overview
Pathogen-associated molecular patterns (PAMPs) trigger host immune response by activating pattern recognition receptors like toll-like receptors (TLRs). However, the mechanism whereby several pathogens, including viruses, activate TLRs via a non-PAMP mechanism is unclear. Endogenous \"inflammatory mediators\" called damage-associated molecular patterns (DAMPs) have been implicated in regulating immune response and inflammation. However, the role of DAMPs in inflammation/immunity during virus infection has not been studied. We have identified a DAMP molecule, S100A9 (also known as Calgranulin B or MRP-14), as an endogenous non-PAMP activator of TLR signaling during influenza A virus (IAV) infection. S100A9 was released from undamaged IAV-infected cells and extracellular S100A9 acted as a critical host-derived molecular pattern to regulate inflammatory response outcome and disease during infection by exaggerating pro-inflammatory response, cell-death and virus pathogenesis. Genetic studies showed that the DDX21-TRIF signaling pathway is required for S100A9 gene expression/production during infection. Furthermore, the inflammatory activity of extracellular S100A9 was mediated by activation of the TLR4-MyD88 pathway. Our studies have thus, underscored the role of a DAMP molecule (i.e. extracellular S100A9) in regulating virus-associated inflammation and uncovered a previously unknown function of the DDX21-TRIF-S100A9-TLR4-MyD88 signaling network in regulating inflammation during infection.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
Adaptor Proteins, Vesicular Transport - genetics
/ Adaptor Proteins, Vesicular Transport - immunology
/ Animals
/ DEAD-box RNA Helicases - genetics
/ DEAD-box RNA Helicases - immunology
/ Dogs
/ Grants
/ Influenza A Virus, H1N1 Subtype - immunology
/ Lungs
/ Madin Darby Canine Kidney Cells
/ Mice
/ Myeloid Differentiation Factor 88 - genetics
/ Myeloid Differentiation Factor 88 - immunology
/ Orthomyxoviridae Infections - genetics
/ Orthomyxoviridae Infections - immunology
/ Orthomyxoviridae Infections - pathology
/ Proteins
/ Rodents
/ Signal Transduction - genetics
/ Signal Transduction - immunology
/ Studies
/ Toll-Like Receptor 4 - genetics
