In:
Journal of Innate Immunity, S. Karger AG, Vol. 11, No. 2 ( 2019), p. 125-135
Kurzfassung:
Bacterial challenge of keratinocytes with the abundant skin commensal 〈 i 〉 Staphylococcus epidermidis 〈 /i 〉 induces distinct innate immune responses, but the underlying molecular mechanisms are still emerging. We report that the aryl hydrocarbon receptor (AhR) was activated in human primary keratinocytes infected with 〈 i 〉 S. epidermidis 〈 /i 〉 , leading to induction of the AhR-responsive gene cytochrome P450 1A1 (CYP1A1). In addition, functional AhR was required for 〈 i 〉 S. epidermidis 〈 /i 〉 -mediated induction of IL-1β expression in keratinocytes. AhR-dependent gene induction of IL-1β and CYP1A1 was mediated by factor(s) & #x3c; 2 kDa secreted by 〈 i 〉 S. epidermidis 〈 /i 〉 . Blockade of the AhR in a 3D organotypic skin equivalent infected with 〈 i 〉 S. epidermidis 〈 /i 〉 attenuated the 〈 i 〉 S. epidermidis 〈 /i 〉 -induced CYP1A1 and IL-1β expression. Moreover, 〈 i 〉 S. epidermidis 〈 /i 〉 also induced expression of IL-1α and of the antimicrobial peptide human β-defensin-3 in an AhR-dependent manner in a 3D skin equivalent. An increased outgrowth of 〈 i 〉 S. epidermidis 〈 /i 〉 on the surface of skin explants treated with a specific AhR inhibitor further indicate a pivotal role of the AhR in mediating an epidermal defense response. Taken together, our data expand the role of the AhR in innate immunity and support a previously unappreciated contribution for the AhR in cutaneous defense.
Materialart:
Online-Ressource
ISSN:
1662-811X
,
1662-8128
Sprache:
Englisch
Verlag:
S. Karger AG
Publikationsdatum:
2019
ZDB Id:
2455818-7
