{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T14:28:58Z","timestamp":1785421738419,"version":"3.56.0"},"reference-count":52,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T00:00:00Z","timestamp":1776211200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T00:00:00Z","timestamp":1776211200000},"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":["R21AI147097"],"award-info":[{"award-number":["R21AI147097"]}],"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":["R21AI144571"],"award-info":[{"award-number":["R21AI144571"]}],"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":["R01AI175461"],"award-info":[{"award-number":["R01AI175461"]}],"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":["P20GM144041"],"award-info":[{"award-number":["P20GM144041"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2026,4,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Infections caused by\n                      <jats:italic toggle=\"yes\">Streptococcus pneumoniae<\/jats:italic>\n                      (\n                      <jats:italic toggle=\"yes\">Spn<\/jats:italic>\n                      , pneumococcus), manifesting as pneumonia, meningitis, and otitis media, represent a leading cause of severe morbidity and mortality globally. Escalating antibiotic resistance and serotype replacement by conjugate vaccines underscore the need for serotype-independent therapies. Hypothiocyanous acid (HOSCN), a reactive oxidant naturally produced by the host innate immune system, is formed through the interaction of hydrogen peroxide, thiocyanate anions (SCN\n                      <jats:sup>\u2212<\/jats:sup>\n                      ), and peroxidase enzymes. HOSCN is produced at mucosal surfaces, including the respiratory epithelium, where it functions as a broad-spectrum oxidative agent. HOSCN has been reported to kill Spn\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      , but tolerance mechanisms of Spn against HOSCN have also been described. This review synthesizes recent advances in understanding HOSCN\u2019s molecular mechanisms of action, tolerance pathways of Spn, and the effects of HOSCN on host-Spn interactions. The article also discusses current limitations and key challenges that must be addressed to translate HOSCN from preclinical promise to clinical application in the management of Spn lung infections. By leveraging an innate microbicidal pathway already active in the healthy lung, HOSCN-based therapeutics could offer rapid, resistance-refractory control of pneumococcal disease.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/iai.00070-26","type":"journal-article","created":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T13:02:56Z","timestamp":1773666176000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["Determinants of susceptibility and tolerance of\n                    <i>Streptococcus pneumoniae<\/i>\n                    to hypothiocyanous acid"],"prefix":"10.1128","volume":"94","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9742-4955","authenticated-orcid":true,"given":"Bal\u00e1zs","family":"Rada","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00te3t702","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Infectious Diseases, College of Veterinary Medicine, The University of Georgia","place":["Athens, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0573-5658","authenticated-orcid":true,"given":"Jorge E.","family":"Vidal","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02teq1165","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Cell and Molecular Biology and Center for Immunology and Microbial Research, School of Medicine, The University of Mississippi Medical Center","place":["Jackson, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","volume-title":"Streptococcus pneumoniae","author":"Dion CF","year":"2025","unstructured":"Dion CF, Ashurst JV. 2025. 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