{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,2]],"date-time":"2026-11-02T22:07:52Z","timestamp":1793657272948,"version":"4.5.1"},"reference-count":48,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2021,10,29]],"date-time":"2021-10-29T00:00:00Z","timestamp":1635465600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["TR156"],"award-info":[{"award-number":["TR156"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["DFG510\/8\u20102"],"award-info":[{"award-number":["DFG510\/8\u20102"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2022,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:italic>Staphylococcus aureus<\/jats:italic> colonization is abundant on the skin of atopic dermatitis (AD) patients where it contributes to skin inflammation. <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> produces virulence factors that distinguish it from commensal skin bacteria such as <jats:italic>S<\/jats:italic>. <jats:italic>epidermidis<\/jats:italic> and <jats:italic>S<\/jats:italic>. <jats:italic>lugdunensis<\/jats:italic>. However, it has remained unclear, which of these virulence factors have the strongest impact on AD. Membrane vesicles (MVs) are released by pathogenic bacteria and might play an essential role in the long\u2010distance delivery of bacterial effectors such as virulence factors. We show that MVs are also released by skin commensals in a similar quantity and membrane lipid amount as those from pathogenic <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic>. Interestingly, MVs from skin commensals can protect against <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> skin colonization by conditioning human skin for enhanced defence. In contrast, MVs released by <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> are able to induce CXCL8 and TNF\u2010\u03b1 in primary human keratinocytes, recruit neutrophils and induce neutrophil extracellular traps, which enhance <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> skin colonization. CXCL8 induction is TLR2\u2010 and NFkB\u2010dependent and the induction level correlates with the membrane lipid and protein A content of the MVs. Interestingly, MVs of <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> strains from the lesional skin of AD patients show an enhanced membrane lipid and protein A content compared to the strains from the non\u2010lesional sites and have an enhanced proinflammatory potential. Our data underline the complex interplay in host\u2010 and bacterial derived factors in <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> skin colonization and the important role of bacterial derived MVs and their membrane lipid and protein A content in skin inflammatory disorders.<\/jats:p>","DOI":"10.1111\/exd.14478","type":"journal-article","created":{"date-parts":[[2021,10,22]],"date-time":"2021-10-22T23:42:05Z","timestamp":1634946125000},"page":"349-361","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Bacterial membrane vesicles shape <i>Staphylococcus aureus<\/i> skin colonization and induction of innate immune responses"],"prefix":"10.1111","volume":"31","author":[{"given":"Lena","family":"Staudenmaier","sequence":"first","affiliation":[{"name":"Department of Dermatology University of T\u00fcbingen T\u00fcbingen Germany"},{"name":"Cluster of Excellence EXC 2124 Controlling Microbes to Fight 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