Asset Details
Do you wish to reserve the book?
Hydrogen sulfide stimulates Mycobacterium tuberculosis respiration, growth and pathogenesis
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Hydrogen sulfide stimulates Mycobacterium tuberculosis respiration, growth and pathogenesis
Do you wish to request the book?
Hydrogen sulfide stimulates Mycobacterium tuberculosis respiration, growth and pathogenesis
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Hydrogen sulfide stimulates Mycobacterium tuberculosis respiration, growth and pathogenesis
2020
Overview
Hydrogen sulfide (H
2
S) is involved in numerous pathophysiological processes and shares overlapping functions with CO and
•
NO. However, the importance of host-derived H
2
S in microbial pathogenesis is unknown. Here we show that
Mtb
-infected mice deficient in the H
2
S-producing enzyme cystathionine β-synthase (CBS) survive longer with reduced organ burden, and that pharmacological inhibition of CBS reduces
Mtb
bacillary load in mice. High-resolution respirometry, transcriptomics and mass spectrometry establish that H
2
S stimulates
Mtb
respiration and bioenergetics predominantly via cytochrome
bd
oxidase, and that H
2
S reverses •NO-mediated inhibition of
Mtb
respiration. Further, exposure of
Mtb
to H
2
S regulates genes involved in sulfur and copper metabolism and the Dos regulon. Our results indicate that
Mtb
exploits host-derived H
2
S to promote growth and disease, and suggest that host-directed therapies targeting H
2
S production may be potentially useful for the management of tuberculosis and other microbial infections.
The importance of host-produced hydrogen sulfide (H
2
S) in microbial pathogenesis is poorly understood. Here, Saini et al. show that H
2
S alters
Mycobacterium tuberculosis
(Mtb) central metabolism, stimulates respiration to promote growth and TB disease, and upregulates the Dos regulon.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/106
/ 13/21
/ 13/31
/ 38/88
/ 38/90
/ 38/91
/ 64/60
/ 82/29
/ 82/58
/ Animals
/ Cystathionine beta-Synthase - genetics
/ Cystathionine beta-Synthase - metabolism
/ Electron Transport Complex IV - metabolism
/ Female
/ Gene Expression Regulation, Bacterial - drug effects
/ Humanities and Social Sciences
/ Hydrogen Sulfide - pharmacology
/ Male
/ Mice
/ Mycobacterium tuberculosis - drug effects
/ Mycobacterium tuberculosis - genetics
/ Mycobacterium tuberculosis - metabolism
/ Mycobacterium tuberculosis - pathogenicity
/ Regulon
/ Science
/ Sulfur
