OAS1, OAS2 and OAS3 restrict intracellular M. tb replication and enhance cytokine secretion
The 2′,5′ (OASs) are known as mediators of the antiviral response system through activation of the RNA cleavage pathway. Interestingly, we observe OAS1, OAS2 and OAS3 upregulation in a number of gene expression signatures which discriminate active TB from latent TB infection, however their biologica...
Main Authors: | , , , |
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Format: | Article |
Language: | English |
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Elsevier
2019-03-01
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Series: | International Journal of Infectious Diseases |
Online Access: | http://www.sciencedirect.com/science/article/pii/S1201971219300931 |
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author | Gina Leisching Victoria Cole Aus T. Ali Bienyameen Baker |
author_facet | Gina Leisching Victoria Cole Aus T. Ali Bienyameen Baker |
author_sort | Gina Leisching |
collection | DOAJ |
description | The 2′,5′ (OASs) are known as mediators of the antiviral response system through activation of the RNA cleavage pathway. Interestingly, we observe OAS1, OAS2 and OAS3 upregulation in a number of gene expression signatures which discriminate active TB from latent TB infection, however their biological role during bacterial infection has not yet been elucidated. We observed that the expression of these genes was associated with pathogenicity and virulence of mycobacteria as infection with Mycobacterium bovis BCG failed to significantly induce OAS expression. Further, we observed that after silencing of these genes, M. tb CFU counts increased significantly 96 h post-infection in comparison to the respective controls. Luminex revealed that OAS silencing significantly decreased IL-1β, TNF-α and MCP-1 and had no effect of IL-10 secretion. We show for the first time that OAS1, 2 and 3 restrict intracellular pathogenic mycobacterial replication and enhance pro-inflammatory cytokine secretion. Keywords: M. tuberculosis, OAS, Host-defence, Anti-microbial, Pathogenesis, Virulence |
first_indexed | 2024-04-14T05:52:46Z |
format | Article |
id | doaj.art-df7b33037a16485f8055dc2e7e455443 |
institution | Directory Open Access Journal |
issn | 1201-9712 |
language | English |
last_indexed | 2024-04-14T05:52:46Z |
publishDate | 2019-03-01 |
publisher | Elsevier |
record_format | Article |
series | International Journal of Infectious Diseases |
spelling | doaj.art-df7b33037a16485f8055dc2e7e4554432022-12-22T02:09:03ZengElsevierInternational Journal of Infectious Diseases1201-97122019-03-0180S77S84OAS1, OAS2 and OAS3 restrict intracellular M. tb replication and enhance cytokine secretionGina Leisching0Victoria Cole1Aus T. Ali2Bienyameen Baker3NRF-DST Centre of Excellence for Biomedical Tuberculosis Research, South African Medical Research Council Centre for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa; Corresponding author.NRF-DST Centre of Excellence for Biomedical Tuberculosis Research, South African Medical Research Council Centre for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South AfricaDepartment of Pathology, National Health Laboratory Service, Tygerberg Hospital, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South AfricaNRF-DST Centre of Excellence for Biomedical Tuberculosis Research, South African Medical Research Council Centre for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South AfricaThe 2′,5′ (OASs) are known as mediators of the antiviral response system through activation of the RNA cleavage pathway. Interestingly, we observe OAS1, OAS2 and OAS3 upregulation in a number of gene expression signatures which discriminate active TB from latent TB infection, however their biological role during bacterial infection has not yet been elucidated. We observed that the expression of these genes was associated with pathogenicity and virulence of mycobacteria as infection with Mycobacterium bovis BCG failed to significantly induce OAS expression. Further, we observed that after silencing of these genes, M. tb CFU counts increased significantly 96 h post-infection in comparison to the respective controls. Luminex revealed that OAS silencing significantly decreased IL-1β, TNF-α and MCP-1 and had no effect of IL-10 secretion. We show for the first time that OAS1, 2 and 3 restrict intracellular pathogenic mycobacterial replication and enhance pro-inflammatory cytokine secretion. Keywords: M. tuberculosis, OAS, Host-defence, Anti-microbial, Pathogenesis, Virulencehttp://www.sciencedirect.com/science/article/pii/S1201971219300931 |
spellingShingle | Gina Leisching Victoria Cole Aus T. Ali Bienyameen Baker OAS1, OAS2 and OAS3 restrict intracellular M. tb replication and enhance cytokine secretion International Journal of Infectious Diseases |
title | OAS1, OAS2 and OAS3 restrict intracellular M. tb replication and enhance cytokine secretion |
title_full | OAS1, OAS2 and OAS3 restrict intracellular M. tb replication and enhance cytokine secretion |
title_fullStr | OAS1, OAS2 and OAS3 restrict intracellular M. tb replication and enhance cytokine secretion |
title_full_unstemmed | OAS1, OAS2 and OAS3 restrict intracellular M. tb replication and enhance cytokine secretion |
title_short | OAS1, OAS2 and OAS3 restrict intracellular M. tb replication and enhance cytokine secretion |
title_sort | oas1 oas2 and oas3 restrict intracellular m tb replication and enhance cytokine secretion |
url | http://www.sciencedirect.com/science/article/pii/S1201971219300931 |
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