Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/53739
Title: FUNCTIONAL CHARACTERIZATION OF ANNEXIN A1 IN TOLL LIKE RECEPTOR 7 SIGNALLING & INFLUENZA VIRUS INFECTION
Authors: SURUCHI ARORA
Keywords: Annexin A1, Influenza, Toll like receptor 7
Issue Date: 22-Jan-2014
Source: SURUCHI ARORA (2014-01-22). FUNCTIONAL CHARACTERIZATION OF ANNEXIN A1 IN TOLL LIKE RECEPTOR 7 SIGNALLING & INFLUENZA VIRUS INFECTION. ScholarBank@NUS Repository.
Abstract: ANXA1 is an immune-modulatory protein and is known to play important role in cell differentiation, adhesion, migration, proliferation and apoptosis. Our lab has already shown its involvement in TLR3 signalling. To follow up this study with the other RNA sensing receptors we chose to investigate the effects of ANXA1 in TLR7 signalling by using an artificial agonist, R848 and a natural ligand Influenza virus. In this project, cytokine production in various cell types with TLR7 agonist R848 was observed which indicated the cell-specificity exhibited by ANXA1, due to which bone marrow macrophages require ANXA1 for cytokine production while bone marrow dendritic cells can produce high amounts of cytokines in its absence. We also established that ANXA1 plays a role in Influenza virus infection and positively regulates virus titers due to which ANXA1-/- mice have greater survival rates compared to WT. No differences are observed in cytokine levels or lung damage. Invitro analysis of viral titers in human alveolar type II epithelial cell line A549, show similar results as observed in vivo. Overexpression of ANXA1 leads to higher viral loads whereas the knockdown reduces viral loads. Apoptosis favours viral propagation and hence higher apoptosis may lead to higher viral loads in the lungs of infected mice. In all, our study shows that ANXA1 plays a detrimental role in the influenza infection and better targeting of the molecule might bring out more efficient therapies against influenza virus.
URI: http://scholarbank.nus.edu.sg/handle/10635/53739
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