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An Accord of Nuclear Receptor Expression in M. tuberculosis Infected Macrophages and Dendritic Cells

Mycobacterium tuberculosis instigates interactions with host factors to promote its survival within the host inimical conditions. Among such factors, nuclear receptors (NRs) seem to be promising candidates owing to their role in bacterial pathogenesis. However, only few members of NR superfamily hav...

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Autores principales: Saini, Ankita, Mahajan, Sahil, Ahuja, Nancy, Bhagyaraj, Ella, Kalra, Rashi, Janmeja, Ashok Kumar, Gupta, Pawan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5797181/
https://www.ncbi.nlm.nih.gov/pubmed/29396519
http://dx.doi.org/10.1038/s41598-018-20769-4
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author Saini, Ankita
Mahajan, Sahil
Ahuja, Nancy
Bhagyaraj, Ella
Kalra, Rashi
Janmeja, Ashok Kumar
Gupta, Pawan
author_facet Saini, Ankita
Mahajan, Sahil
Ahuja, Nancy
Bhagyaraj, Ella
Kalra, Rashi
Janmeja, Ashok Kumar
Gupta, Pawan
author_sort Saini, Ankita
collection PubMed
description Mycobacterium tuberculosis instigates interactions with host factors to promote its survival within the host inimical conditions. Among such factors, nuclear receptors (NRs) seem to be promising candidates owing to their role in bacterial pathogenesis. However, only few members of NR superfamily have been implicated in M. tuberculosis infection and there is a dearth of comprehensive knowledge about expression or function of the entire superfamily. In this study, we performed detailed expression analysis and identified key NRs getting differentially regulated in murine macrophages and dendritic cells (DC) upon infection with H37Rv. The murine macrophages and DCs infected with H37Rv entailed overlapping changes in the expression of certain NRs which reflect upon the possibility that both cells might utilize similar transcriptional programs upon M. tuberculosis infection. We identified Nr4a3 and Rora, which have not been implicated in M. tuberculosis pathogenesis, undergo similar changes in expression in macrophages and DCs upon H37Rv infection. Interestingly, a similar pattern in their expression was also observed in infected human monocyte derived macrophages and the findings corroborated well with PBMCs obtained from TB patients. This all-inclusive analysis provides the basis for a precise approach in identifying NRs that can be targeted therapeutically in intracellular bacterial infections.
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spelling pubmed-57971812018-02-13 An Accord of Nuclear Receptor Expression in M. tuberculosis Infected Macrophages and Dendritic Cells Saini, Ankita Mahajan, Sahil Ahuja, Nancy Bhagyaraj, Ella Kalra, Rashi Janmeja, Ashok Kumar Gupta, Pawan Sci Rep Article Mycobacterium tuberculosis instigates interactions with host factors to promote its survival within the host inimical conditions. Among such factors, nuclear receptors (NRs) seem to be promising candidates owing to their role in bacterial pathogenesis. However, only few members of NR superfamily have been implicated in M. tuberculosis infection and there is a dearth of comprehensive knowledge about expression or function of the entire superfamily. In this study, we performed detailed expression analysis and identified key NRs getting differentially regulated in murine macrophages and dendritic cells (DC) upon infection with H37Rv. The murine macrophages and DCs infected with H37Rv entailed overlapping changes in the expression of certain NRs which reflect upon the possibility that both cells might utilize similar transcriptional programs upon M. tuberculosis infection. We identified Nr4a3 and Rora, which have not been implicated in M. tuberculosis pathogenesis, undergo similar changes in expression in macrophages and DCs upon H37Rv infection. Interestingly, a similar pattern in their expression was also observed in infected human monocyte derived macrophages and the findings corroborated well with PBMCs obtained from TB patients. This all-inclusive analysis provides the basis for a precise approach in identifying NRs that can be targeted therapeutically in intracellular bacterial infections. Nature Publishing Group UK 2018-02-02 /pmc/articles/PMC5797181/ /pubmed/29396519 http://dx.doi.org/10.1038/s41598-018-20769-4 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Saini, Ankita
Mahajan, Sahil
Ahuja, Nancy
Bhagyaraj, Ella
Kalra, Rashi
Janmeja, Ashok Kumar
Gupta, Pawan
An Accord of Nuclear Receptor Expression in M. tuberculosis Infected Macrophages and Dendritic Cells
title An Accord of Nuclear Receptor Expression in M. tuberculosis Infected Macrophages and Dendritic Cells
title_full An Accord of Nuclear Receptor Expression in M. tuberculosis Infected Macrophages and Dendritic Cells
title_fullStr An Accord of Nuclear Receptor Expression in M. tuberculosis Infected Macrophages and Dendritic Cells
title_full_unstemmed An Accord of Nuclear Receptor Expression in M. tuberculosis Infected Macrophages and Dendritic Cells
title_short An Accord of Nuclear Receptor Expression in M. tuberculosis Infected Macrophages and Dendritic Cells
title_sort accord of nuclear receptor expression in m. tuberculosis infected macrophages and dendritic cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5797181/
https://www.ncbi.nlm.nih.gov/pubmed/29396519
http://dx.doi.org/10.1038/s41598-018-20769-4
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