{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T12:55:33Z","timestamp":1791204933941,"version":"4.1.0"},"reference-count":15,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T00:00:00Z","timestamp":1790640000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T00:00:00Z","timestamp":1790640000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01AI125588"],"award-info":[{"award-number":["R01AI125588"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["P01AI083211"],"award-info":[{"award-number":["P01AI083211"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01AI192812"],"award-info":[{"award-number":["R01AI192812"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000057","name":"National Institute of General Medical Sciences","doi-asserted-by":"publisher","award":["1R35GM154838"],"award-info":[{"award-number":["1R35GM154838"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["25PRE1369371"],"award-info":[{"award-number":["25PRE1369371"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000057","name":"National Institute of General Medical Sciences","doi-asserted-by":"publisher","award":["1T32GM153375-01"],"award-info":[{"award-number":["1T32GM153375-01"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mSphere"],"published-print":{"date-parts":[[2026,9,29]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Hypochlorous acid (HOCl) is a potent antimicrobial oxidant produced by innate immune cells to eliminate invading bacterial pathogens, including\n                      <jats:italic toggle=\"yes\">Staphylococcus aureus<\/jats:italic>\n                      . HOCl readily oxidizes thiols, amines, and macromolecules in\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      . Yet, some bacterial cells within an HOCl-challenged population withstand this oxidative stress and proceed to establish infection. The mechanisms that enable\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      to resist the effects of HOCl remain incompletely understood. Here, we show that cysteine uptake is a major determinant of HOCl resistance in\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      . Inactivation of the cysteine transporters\n                      <jats:italic toggle=\"yes\">tcyABC<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">tcyP<\/jats:italic>\n                      resulted in a dose-dependent increase in sensitivity to HOCl. Cysteine uptake through these transporters helped maintain bacillithiol homeostasis and limit oxidative damage to protein thiols during HOCl stress. Importantly, cysteine uptake was required for the survival of\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      during interaction with activated human neutrophils that generate HOCl to kill phagocytosed bacteria. These findings reveal that cysteine uptake expands the thiol buffering capacity of\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      and functions as a major mechanism for scavenging HOCl, which may contribute to its persistence in the infected host.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        <jats:italic toggle=\"yes\">Staphylococcus aureus<\/jats:italic>\n                        is a major human pathogen that causes recurrent and antibiotic-recalcitrant infections. Understanding the mechanisms that allow\n                        <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                        to evade key innate immune defenses is therefore of considerable interest for developing effective intervention strategies. Our findings show that cysteine uptake is a critical component of\n                        <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                        defense against hypochlorous acid (HOCl) produced by innate immune cells. Cysteine functions as a reactive sink for HOCl and thereby prevents depletion of both low-molecular-weight thiols and protein thiols in\n                        <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                        .\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/msphere.00214-26","type":"journal-article","created":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T13:06:50Z","timestamp":1787576810000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Cysteine import contributes to hypochlorous acid resistance in\n                    <i>Staphylococcus aureus<\/i>"],"prefix":"10.1128","volume":"11","author":[{"given":"Abigail G.","family":"Hall","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00thqtb16","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Pathology, Microbiology and Immunology, Center for Staphylococcal Research, University of Nebraska Medical Center","place":["Omaha, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aliyah J.","family":"Collins","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/020f3ap87","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, University of Tennessee","place":["Knoxville, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna","family":"Sommers","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00thqtb16","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Pathology, Microbiology and Immunology, Center for Staphylococcal Research, University of Nebraska Medical Center","place":["Omaha, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9711-1951","authenticated-orcid":true,"given":"Ryan","family":"Singh","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00thqtb16","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Pathology, Microbiology and Immunology, Center for Staphylococcal Research, University of Nebraska Medical Center","place":["Omaha, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sasmita","family":"Panda","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00thqtb16","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Pathology, Microbiology and Immunology, Center for Staphylococcal Research, University of Nebraska Medical Center","place":["Omaha, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9609-152X","authenticated-orcid":false,"given":"Sujata S.","family":"Chaudhari","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00thqtb16","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Pathology, Microbiology and Immunology, Center for Staphylococcal Research, University of Nebraska Medical Center","place":["Omaha, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7259-6574","authenticated-orcid":true,"given":"Andrew J.","family":"Monteith","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/020f3ap87","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, University of Tennessee","place":["Knoxville, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7886-0727","authenticated-orcid":true,"given":"Vinai 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