Reactivation of latent tuberculosis through modulation of resuscitation promoting factors by diabetes

Abstract The evidence of an association between diabetes and latent tuberculosis infection (LTBI) remains limited and inconsistent. Thus, the study aims to delineate the role of diabetes in activation of latent tuberculosis infection. Murine model of latent tuberculosis and diabetes was developed, b...

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Autores principales:	Arpana Verma, Maninder Kaur, Lakshya Veer Singh, Divya Aggarwal, Indu Verma, Bishan D. Radotra, Sadhna Sharma
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/2a29c70e85d94ca88c3090afc9c7d68f
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spelling	oai:doaj.org-article:2a29c70e85d94ca88c3090afc9c7d68f2021-12-02T18:37:09ZReactivation of latent tuberculosis through modulation of resuscitation promoting factors by diabetes10.1038/s41598-021-99257-12045-2322https://doaj.org/article/2a29c70e85d94ca88c3090afc9c7d68f2021-10-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-99257-1https://doaj.org/toc/2045-2322Abstract The evidence of an association between diabetes and latent tuberculosis infection (LTBI) remains limited and inconsistent. Thus, the study aims to delineate the role of diabetes in activation of latent tuberculosis infection. Murine model of latent tuberculosis and diabetes was developed, bacillary load and gene expression of resuscitation promoting factors (rpfA-E) along with histopathological changes in the lungs and spleen were studied. Treatment for LTBI [Rifampicin (RIF) + Isoniazid (INH)] was also given to latently infected mice with or without diabetes for 4 weeks. Diabetes was found to activate latent tuberculosis as the colony forming unit (CFU) counts were observed to be > 104 in lungs and spleen. The gene expression of hspX was downregulated and that of rpfB and rpfD was observed to be upregulated in latently infected mice with diabetes compared to those without diabetes. However, no significant reduction in the CFU counts was observed after 4 weeks of treatment with RIF and INH. Diabetes helps in the progression of LTBI to active disease mainly through altered expression of resuscitation promoting factors rpfB and rpfD, which can serve as important targets to reduce the shared burden of tuberculosis and diabetes.Arpana VermaManinder KaurLakshya Veer SinghDivya AggarwalIndu VermaBishan D. RadotraSadhna SharmaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Arpana Verma Maninder Kaur Lakshya Veer Singh Divya Aggarwal Indu Verma Bishan D. Radotra Sadhna Sharma Reactivation of latent tuberculosis through modulation of resuscitation promoting factors by diabetes
description	Abstract The evidence of an association between diabetes and latent tuberculosis infection (LTBI) remains limited and inconsistent. Thus, the study aims to delineate the role of diabetes in activation of latent tuberculosis infection. Murine model of latent tuberculosis and diabetes was developed, bacillary load and gene expression of resuscitation promoting factors (rpfA-E) along with histopathological changes in the lungs and spleen were studied. Treatment for LTBI [Rifampicin (RIF) + Isoniazid (INH)] was also given to latently infected mice with or without diabetes for 4 weeks. Diabetes was found to activate latent tuberculosis as the colony forming unit (CFU) counts were observed to be > 104 in lungs and spleen. The gene expression of hspX was downregulated and that of rpfB and rpfD was observed to be upregulated in latently infected mice with diabetes compared to those without diabetes. However, no significant reduction in the CFU counts was observed after 4 weeks of treatment with RIF and INH. Diabetes helps in the progression of LTBI to active disease mainly through altered expression of resuscitation promoting factors rpfB and rpfD, which can serve as important targets to reduce the shared burden of tuberculosis and diabetes.
format	article
author	Arpana Verma Maninder Kaur Lakshya Veer Singh Divya Aggarwal Indu Verma Bishan D. Radotra Sadhna Sharma
author_facet	Arpana Verma Maninder Kaur Lakshya Veer Singh Divya Aggarwal Indu Verma Bishan D. Radotra Sadhna Sharma
author_sort	Arpana Verma
title	Reactivation of latent tuberculosis through modulation of resuscitation promoting factors by diabetes
title_short	Reactivation of latent tuberculosis through modulation of resuscitation promoting factors by diabetes
title_full	Reactivation of latent tuberculosis through modulation of resuscitation promoting factors by diabetes
title_fullStr	Reactivation of latent tuberculosis through modulation of resuscitation promoting factors by diabetes
title_full_unstemmed	Reactivation of latent tuberculosis through modulation of resuscitation promoting factors by diabetes
title_sort	reactivation of latent tuberculosis through modulation of resuscitation promoting factors by diabetes
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/2a29c70e85d94ca88c3090afc9c7d68f
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Reactivation of latent tuberculosis through modulation of resuscitation promoting factors by diabetes

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