| First Author | Saini V | Year | 2020 |
| Journal | Nat Commun | Volume | 11 |
| Issue | 1 | Pages | 557 |
| PubMed ID | 31992699 | Mgi Jnum | J:289826 |
| Mgi Id | MGI:6387500 | Doi | 10.1038/s41467-019-14132-y |
| Citation | Saini V, et al. (2020) Hydrogen sulfide stimulates Mycobacterium tuberculosis respiration, growth and pathogenesis. Nat Commun 11(1):557 |
| abstractText | Hydrogen sulfide (H2S) is involved in numerous pathophysiological processes and shares overlapping functions with CO and *NO. However, the importance of host-derived H2S in microbial pathogenesis is unknown. Here we show that Mtb-infected mice deficient in the H2S-producing enzyme cystathionine beta-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 H2S stimulates Mtb respiration and bioenergetics predominantly via cytochrome bd oxidase, and that H2S reverses *NO-mediated inhibition of Mtb respiration. Further, exposure of Mtb to H2S regulates genes involved in sulfur and copper metabolism and the Dos regulon. Our results indicate that Mtb exploits host-derived H2S to promote growth and disease, and suggest that host-directed therapies targeting H2S production may be potentially useful for the management of tuberculosis and other microbial infections. |
