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. 2020 Jan 28;11:557. doi: 10.1038/s41467-019-14132-y

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© The Author(s) 2020

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/.

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Fig. 7 — a As a response to Mtb infection, the host increases CBS and H₂S production in the lungs and macrophages leading to increased bacillary burden, increased inflammation, and reduced survival. b Host-generated H₂S is sensed by Mtb to stimulate respiration and energy metabolism, thereby increasing bacterial growth and accelerating disease. During infection, increased H₂S suppresses iNOS levels and production of •NO. H₂S also mitigates the bacteriostatic effect of •NO on Mtb respiration. Green arrows represent increase; red arrows represent decrease.