Hydrogen sulfide dysregulates the immune response by suppressing central carbon metabolism to promote tuberculosis.

ABSTRACT: The ubiquitous gasotransmitter hydrogen sulfide (H₂S) has been recognized to play a crucial role in human health. Using cystathionine γ-lyase (CSE)-deficient mice, we demonstrate an unexpected role of H₂S in Mycobacterium tuberculosis (Mtb) pathogenesis. We showed that Mtb-infected CSE^-/- mice survive longer than WT mice, and support reduced pathology and lower bacterial burdens in the lung, spleen, and liver. Similarly, in vitro Mtb infection of macrophages resulted in reduced colony forming units in CSE^-/- cells. Chemical complementation of infected WT and CSE^-/- macrophages using the slow H₂S releaser GYY3147 and the CSE inhibitor DL-propargylglycine demonstrated that H₂S is the effe

SUBMITTER: Rahman MA 

PROVIDER: S-EPMC7104411 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature