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Understanding the dynamics of Toll-like Receptor 5 response to flagellin and its regulation by estradiol

Toll-like receptors (TLRs) are major players of the innate immune system. Once activated, they trigger a signalling cascade that leads to NF-κB translocation from the cytoplasm to the nucleus. Single cell analysis shows that NF-κB signalling dynamics are a critical determinant of transcriptional reg...

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Published in:Scientific reports 2017-01, Vol.7 (1), p.40981, Article 40981
Main Authors: Caballero, Ignacio, Boyd, James, Almiñana, Carmen, Sánchez-López, Javier A., Basatvat, Shaghayegh, Montazeri, Mehrnaz, Maslehat Lay, Nasim, Elliott, Sarah, Spiller, David G., White, Michael R. H., Fazeli, Alireza
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cited_by cdi_FETCH-LOGICAL-c472t-59e00b2cf356d4a339a4d91a08d905df4bca6162e2dd7dc40877b0b3a5b94eda3
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container_title Scientific reports
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creator Caballero, Ignacio
Boyd, James
Almiñana, Carmen
Sánchez-López, Javier A.
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Elliott, Sarah
Spiller, David G.
White, Michael R. H.
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description Toll-like receptors (TLRs) are major players of the innate immune system. Once activated, they trigger a signalling cascade that leads to NF-κB translocation from the cytoplasm to the nucleus. Single cell analysis shows that NF-κB signalling dynamics are a critical determinant of transcriptional regulation. Moreover, the outcome of innate immune response is also affected by the cross-talk between TLRs and estrogen signalling. Here, we characterized the dynamics of TLR5 signalling, responsible for the recognition of flagellated bacteria, and those changes induced by estradiol in its signalling at the single cell level. TLR5 activation in MCF7 cells induced a single and sustained NF-κB translocation into the nucleus that resulted in high NF-κB transcription activity. The overall magnitude of NF-κB transcription activity was not influenced by the duration of the stimulus. No significant changes are observed in the dynamics of NF-κB translocation to the nucleus when MCF7 cells are incubated with estradiol. However, estradiol significantly decreased NF-κB transcriptional activity while increasing TLR5-mediated AP-1 transcription. The effect of estradiol on transcriptional activity was dependent on the estrogen receptor activated. This fine tuning seems to occur mainly in the nucleus at the transcription level rather than affecting the translocation of the NF-κB transcription factor.
doi_str_mv 10.1038/srep40981
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H.</creatorcontrib><creatorcontrib>Fazeli, Alireza</creatorcontrib><title>Understanding the dynamics of Toll-like Receptor 5 response to flagellin and its regulation by estradiol</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Toll-like receptors (TLRs) are major players of the innate immune system. Once activated, they trigger a signalling cascade that leads to NF-κB translocation from the cytoplasm to the nucleus. Single cell analysis shows that NF-κB signalling dynamics are a critical determinant of transcriptional regulation. Moreover, the outcome of innate immune response is also affected by the cross-talk between TLRs and estrogen signalling. Here, we characterized the dynamics of TLR5 signalling, responsible for the recognition of flagellated bacteria, and those changes induced by estradiol in its signalling at the single cell level. 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subjects 13/106
13/44
13/95
14/19
14/35
17β-Estradiol
38/109
38/77
631/250/262/2106
631/250/262/2106/2108
Activator protein 1
Cell activation
Cytoplasm
Estradiol - metabolism
Estrogens
Estrogens - metabolism
Flagellin
Flagellin - metabolism
Gene Expression Regulation - drug effects
Gene regulation
Humanities and Social Sciences
Humans
Immune response
Immune system
Immunology
Innate immunity
Life Sciences
MCF-7 Cells
multidisciplinary
NF-kappa B - metabolism
Protein Transport
Science
Science (multidisciplinary)
Signal Transduction - drug effects
Single-Cell Analysis
TLR5 protein
Toll-Like Receptor 5 - metabolism
Toll-like receptors
Transcription factors
Transcription, Genetic
Translocation
title Understanding the dynamics of Toll-like Receptor 5 response to flagellin and its regulation by estradiol
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