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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2020,3,24]]},"abstract":"<jats:p>\n                    The ubiquitous gasotransmitter hydrogen sulfide (H\n                    <jats:sub>2<\/jats:sub>\n                    S) has been recognized to play a crucial role in human health. Using cystathionine \u03b3-lyase (CSE)-deficient mice, we demonstrate an unexpected role of H\n                    <jats:sub>2<\/jats:sub>\n                    S in\n                    <jats:italic>Mycobacterium tuberculosis<\/jats:italic>\n                    (\n                    <jats:italic>Mtb<\/jats:italic>\n                    ) pathogenesis. We showed that\n                    <jats:italic>Mtb-<\/jats:italic>\n                    infected CSE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice survive longer than WT mice, and support reduced pathology and lower bacterial burdens in the lung, spleen, and liver. Similarly, in vitro\n                    <jats:italic>Mtb<\/jats:italic>\n                    infection of macrophages resulted in reduced colony forming units in CSE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    cells. Chemical complementation of infected WT and CSE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    macrophages using the slow H\n                    <jats:sub>2<\/jats:sub>\n                    S releaser GYY3147 and the CSE inhibitor DL-propargylglycine demonstrated that H\n                    <jats:sub>2<\/jats:sub>\n                    S is the effector molecule regulating\n                    <jats:italic>Mtb<\/jats:italic>\n                    survival in macrophages. Furthermore, we demonstrate that CSE promotes an excessive innate immune response, suppresses the adaptive immune response, and reduces circulating IL-1\u03b2, IL-6, TNF-\u03b1, and IFN-\u03b3 levels in response to\n                    <jats:italic>Mtb<\/jats:italic>\n                    infection. Notably,\n                    <jats:italic>Mtb<\/jats:italic>\n                    infected CSE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    macrophages show increased flux through glycolysis and the pentose phosphate pathway, thereby establishing a critical link between H\n                    <jats:sub>2<\/jats:sub>\n                    S and central metabolism. Our data suggest that excessive H\n                    <jats:sub>2<\/jats:sub>\n                    S produced by the infected WT mice reduce HIF-1\u03b1 levels, thereby suppressing glycolysis and production of IL-1\u03b2, IL-6, and IL-12, and increasing bacterial burden. Clinical relevance was demonstrated by the spatial distribution of H\n                    <jats:sub>2<\/jats:sub>\n                    S-producing enzymes in human necrotic, nonnecrotic, and cavitary pulmonary tuberculosis (TB) lesions. In summary, CSE exacerbates TB pathogenesis by altering immunometabolism in mice and inhibiting CSE or modulating glycolysis are potential targets for host-directed TB control.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1919211117","type":"journal-article","created":{"date-parts":[[2020,3,5]],"date-time":"2020-03-05T19:55:22Z","timestamp":1583438122000},"page":"6663-6674","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":80,"title":["Hydrogen sulfide dysregulates the immune response by suppressing central carbon metabolism to promote tuberculosis"],"prefix":"10.1073","volume":"117","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2616-3372","authenticated-orcid":false,"given":"Md. Aejazur","family":"Rahman","sequence":"first","affiliation":[{"name":"Africa Health Research Institute, 4001 Durban, KwaZulu Natal, South Africa;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6977-765X","authenticated-orcid":false,"given":"Bridgette M.","family":"Cumming","sequence":"additional","affiliation":[{"name":"Africa Health Research Institute, 4001 Durban, KwaZulu Natal, South Africa;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kelvin W.","family":"Addicott","sequence":"additional","affiliation":[{"name":"Africa Health Research Institute, 4001 Durban, KwaZulu Natal, South Africa;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hayden T.","family":"Pacl","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shannon L.","family":"Russell","sequence":"additional","affiliation":[{"name":"Africa Health Research Institute, 4001 Durban, KwaZulu Natal, South Africa;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kievershen","family":"Nargan","sequence":"additional","affiliation":[{"name":"Africa Health Research Institute, 4001 Durban, KwaZulu Natal, South Africa;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Threnesan","family":"Naidoo","sequence":"additional","affiliation":[{"name":"Department of Anatomical Pathology, National Health Laboratory Service, Inkosi Albert Luthuli Central Hospital, University of KwaZulu-Natal, 4091 Durban, South Africa;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pratistadevi K.","family":"Ramdial","sequence":"additional","affiliation":[{"name":"Department of Anatomical Pathology, National Health Laboratory Service, Inkosi Albert Luthuli Central Hospital, University of KwaZulu-Natal, 4091 Durban, South Africa;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John H.","family":"Adamson","sequence":"additional","affiliation":[{"name":"Africa Health Research Institute, 4001 Durban, KwaZulu Natal, South Africa;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Biology, York University, Toronto, ON M3J 1P3, Canada;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9177-8827","authenticated-orcid":false,"given":"Adrie J. 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