Immune Response to Seasonal Influenza A Virus Infection: A Proteomic Approach

Teran, Luis M.; Rüggeberg, Sabrina; Santiago, Julio; Fuentes-Arenas, Felipe; Hernández, José L.; Montes-Vizuet, A. Rosalía; Li, Xinping; Franz, Thomas

doi:10.1016/j.arcmed.2012.08.008

Cited by 16 publications

(12 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our studies are the first to highlight the role of S100A9 protein and DDX21-TRIF-S100A9-TLR4-MyD88 signaling network in modulating inflammation during virus infection. The clinical significance of our study is borne out by detection of S100A9 protein in mucosal secretions from IAV-infected individuals [73]. The clinical significance of utilizing neutralizing antibody is obvious from possible passive immunization with S100A9 antibody (as shown in Figure 9A and B and S9C) as a new therapeutic strategy to control lung inflammation and associated lung disease during IAV infection.…”

Section: Discussionmentioning

confidence: 86%

DAMP Molecule S100A9 Acts as a Molecular Pattern to Enhance Inflammation during Influenza A Virus Infection: Role of DDX21-TRIF-TLR4-MyD88 Pathway

et al. 2014

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 86%

DAMP Molecule S100A9 Acts as a Molecular Pattern to Enhance Inflammation during Influenza A Virus Infection: Role of DDX21-TRIF-TLR4-MyD88 Pathway

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Bpifa1 (PLUNC) is widely distributed in human nasal lavage fluid (Ghafouri et al , ), nasal mucous (Casado et al , ) and saliva in edentulous patients with type 2 diabetes (Border et al , ). The upregulation of PLUNC has also been reported in salivary glands of HIV‐infected patients (da Silva et al , ), in nasal aspirates following infection of influenza virus (Teran et al , ) and in nasal respiratory epithelium after olfactory bulbectomy in rats (Sung et al , ). These functions might be related to innate immune reactions.…”

Section: Discussionmentioning

confidence: 76%

Upregulation of Bpifb1 expression in the parotid glands of non‐obese diabetic mice

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Nevertheless, these studies often enable valuable protracted longitudinal sampling on the same patient. Building upon previous microarray data sets [47,48], Wang and co-workers [49] applied a multivariate estimation technique (MSET) for H3N2 and H1N1 human infection. The authors were able to monitor the acute phase of infection and quantify the predicted health outcome of infection from the blood of patients.…”

Section: Host Response Models Of Iav Infectionmentioning

confidence: 99%

Influenza-Omics and the Host Response: Recent Advances and Future Prospects

Powell

Waters

2017

Pathogens

View full text Add to dashboard Cite

Influenza A viruses (IAV) continually evolve and have the capacity to cause global pandemics. Because IAV represents an ongoing threat, identifying novel therapies and host innate immune factors that contribute to IAV pathogenesis is of considerable interest. This review summarizes the relevant literature as it relates to global host responses to influenza infection at both the proteome and transcriptome level. The various-omics infection systems that include but are not limited to ferrets, mice, pigs, and even the controlled infection of humans are reviewed. Discussion focuses on recent advances, remaining challenges, and knowledge gaps as it relates to influenza-omics infection outcomes.

show abstract

Immune Response to Seasonal Influenza A Virus Infection: A Proteomic Approach

Cited by 16 publications

References 38 publications

DAMP Molecule S100A9 Acts as a Molecular Pattern to Enhance Inflammation during Influenza A Virus Infection: Role of DDX21-TRIF-TLR4-MyD88 Pathway

DAMP Molecule S100A9 Acts as a Molecular Pattern to Enhance Inflammation during Influenza A Virus Infection: Role of DDX21-TRIF-TLR4-MyD88 Pathway

Upregulation of Bpifb1 expression in the parotid glands of non‐obese diabetic mice

Influenza-Omics and the Host Response: Recent Advances and Future Prospects

Contact Info

Product

Resources

About