{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T18:31:46Z","timestamp":1786559506415,"version":"build-2736575974"},"reference-count":62,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T00:00:00Z","timestamp":1779235200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T00:00:00Z","timestamp":1779235200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Individuals with atopic dermatitis (AD) are at increased risk for skin infections, including eczema herpeticum (EH), a severe condition caused by herpes simplex virus type 1 (HSV\u20101). While AD skin is often colonized by\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>Staphylococcus aureus<\/jats:italic>\n                      <\/jats:styled-content>\n                      (\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>S. aureus<\/jats:italic>\n                      <\/jats:styled-content>\n                      ), its role in EH susceptibility remains unclear. Here we aim to investigate differences in the skin microbiome of AD patients with (ADEH\n                      <jats:sup>+<\/jats:sup>\n                      ) and without (ADEH\n                      <jats:sup>\u2212<\/jats:sup>\n                      ) EH and examine the impact of\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>S. aureus<\/jats:italic>\n                      <\/jats:styled-content>\n                      and\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>S. epidermidis<\/jats:italic>\n                      <\/jats:styled-content>\n                      on HSV\u20101 infection in an in\u00a0vitro keratinocyte model.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      16S microbiome sequencing was performed on skin samples from ADEH\n                      <jats:sup>+<\/jats:sup>\n                      , ADEH\n                      <jats:sup>\u2212<\/jats:sup>\n                      , and healthy controls. To investigate microbial effects on HSV\u20101 infection, keratinocytes were pre\u2010incubated with heat\u2010killed\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>S. aureus<\/jats:italic>\n                      <\/jats:styled-content>\n                      (HKSA) or\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>S. epidermidis<\/jats:italic>\n                      <\/jats:styled-content>\n                      (HKSE), followed by HSV\u20101 infection in the presence or absence of the Th2 cytokines IL\u20104 and IL\u201013, simulating the conditions of AD lesional skin. Infection rates and transcriptomic changes were analyzed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      ADEH\n                      <jats:sup>+<\/jats:sup>\n                      patients showed a reduced microbial diversity compared to ADEH\n                      <jats:sup>\u2212<\/jats:sup>\n                      , with increased\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>S. aureus<\/jats:italic>\n                      <\/jats:styled-content>\n                      and\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>S. epidermidis<\/jats:italic>\n                      <\/jats:styled-content>\n                      colonization. HKSA, but not HKSE, protected keratinocytes from HSV\u20101 infection and reduced the release of infectious progeny virus. Transcriptome analysis of keratinocytes revealed HKSA\u2010induced upregulation of interferon pathways and antimicrobial peptides, and downregulation of HSV\u20101 entry factors.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Pre\u2010incubation with\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>S. aureus<\/jats:italic>\n                      <\/jats:styled-content>\n                      set basal keratinocytes into an alarmed state, restricting HSV\u20101 infection presumably via downregulation of receptors important for viral entry and activation of antiviral pathways.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/all.70392","type":"journal-article","created":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T09:16:02Z","timestamp":1779268562000},"page":"2843-2857","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Keratinocyte Priming by\n                    <i>Staphylococcus aureus<\/i>\n                    Reduces\n                    <scp>HSV<\/scp>\n                    \u20101 Susceptibility"],"prefix":"10.1111","volume":"81","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-1909-1865","authenticated-orcid":false,"given":"Phila Cara","family":"Baumann","sequence":"first","affiliation":[{"name":"Department of Dermatology and Allergy Hannover Medical School  Hannover 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