{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T13:24:16Z","timestamp":1788269056540,"version":"build-2803163510"},"reference-count":34,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["UMAI151958"],"award-info":[{"award-number":["UMAI151958"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["U19AI117673"],"award-info":[{"award-number":["U19AI117673"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["U01AI178772"],"award-info":[{"award-number":["U01AI178772"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["U01AI152011"],"award-info":[{"award-number":["U01AI152011"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Microbiol Spectr"],"published-print":{"date-parts":[[2026,9,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Atopic dermatitis (AD) is a chronic pruritic skin condition characterized by lesions associated with colonization and infection by\n                      <jats:italic toggle=\"yes\">Staphylococcus aureus<\/jats:italic>\n                      . There is growing evidence that\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      contributes to symptoms and persistence of AD through production of cytotoxins, superantigens, and proteases. When AD is treated with the interleukin-4 receptor blocking antibody, dupilumab,\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      colonization declines rapidly. Here, we examined the possible involvement of the host lysozyme-mediated innate immune response in helping to control\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      burden in AD patients.\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      is not killed by lysozyme, but the molecule inhibits\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      exotoxin and exoenzyme (exoprotein) production. Reduced\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      abundance during dupilumab treatment correlated positively with reduced lysozyme levels.\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      colonization and lysozyme levels were not altered in placebo-treated participants until they entered the open-label phase of the study (non-blinded phase) when all participants were treated with dupilumab. During that phase, the\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      and lysozyme levels declined. These findings suggest that AD patients may respond to cutaneous\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      colonization by upregulating lysozyme production.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Staphylococcus aureus<\/jats:italic>\n                      is increasingly viewed as an important contributor to atopic dermatitis (AD) persistence. The host responds to AD by producing cationic peptides, including lysozyme. Lysozyme cannot kill\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      , but the innate defense molecule downregulates exotoxin and exoenzyme production, limiting S. aureus-induced inflammation. Clinical improvement of AD likely requires balancing the inflammatory cascades induced by\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      versus host innate immunity.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/spectrum.01585-26","type":"journal-article","created":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T13:01:30Z","timestamp":1786453290000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Innate host defense lysozyme may help control\n                    <i>Staphylococcus aureus<\/i>\n                    in atopic dermatitis"],"prefix":"10.1128","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8314-9369","authenticated-orcid":false,"given":"Patrick M.","family":"Schlievert","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/036jqmy94","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa","place":["Iowa City, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samuel H.","family":"Kilgore","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/036jqmy94","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa","place":["Iowa City, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Evgeny","family":"Berdyshev","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/016z2bp30","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Medicine, National Jewish Health","place":["Denver, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Nodzenski","sequence":"additional","affiliation":[{"name":"Rho, Inc.","place":["Durham, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gloria","family":"David","sequence":"additional","affiliation":[{"name":"Rho, Inc.","place":["Durham, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takeshi","family":"Yoshida","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00trqv719","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Dermatology, University of Rochester Medical Center","place":["Rochester, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8452-667X","authenticated-orcid":true,"given":"Lisa A.","family":"Beck","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00trqv719","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Dermatology, University of Rochester Medical Center","place":["Rochester, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donald Y. 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