TY  - JOUR
A1  - Haferland, Isabel
A1  - Wallenwein, Chantal M.
A1  - Ickelsheimer, Tanja
A1  - Diehl, Sandra
A1  - Wacker, Matthias
A1  - Schiffmann, Susanne
A1  - Bürger, Claudia
A1  - Kaufmann, Roland
A1  - König, Anke
A1  - Pinter, Andreas
T1  - Mechanism of anti-inflammatory effects of rifampicin in an ex vivo culture system of hidradenitis suppurativa
T2  - Experimental dermatology
N2  - Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease of the hair follicles leading to painful lesions, associated with increased levels of pro-inflammatory cytokines. Numerous guidelines recommend antibiotics like clindamycin and rifampicin in combination, as first-line systemic therapy in moderate-to-severe forms of inflammation. HS has been proposed to be mainly an auto-inflammatory disease associated with but not initially provoked by bacteria. Therefore, it has to be assumed that the pro-inflammatory milieu previously observed in HS skin is not solely dampened by the bacteriostatic inhibition of DNA-dependent RNA polymerase. To further clarify the mechanism of anti-inflammatory effects of rifampicin, ex vivo explants of lesional HS from 8 HS patients were treated with rifampicin, and its effect on cytokine production, immune cells as well as the expression of Toll-like receptor 2 (TLR2) were investigated. Analysis of cell culture medium of rifampicin-treated HS explants revealed an anti-inflammatory effect of rifampicin that significantly inhibiting interleukin (IL)-1β, IL-6, IL-8, IL-10 and tumour necrosis factor (TNF)-α production. Immunohistochemistry of the rifampicin-treated explants suggested a tendency for it to reduce the expression of TLR2 while not affecting the number of immune cells.
KW  - anti-bacterial agents
KW  - anti-inflammatory agent
KW  - hidradenitis suppurativa
KW  - rifampin
KW  - therapeutics
Y1  - 2022
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/75362
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-753627
SN  - 1600-0625
N1  - Open access funding enabled and organized by Projekt DEAL.
VL  - 31
IS  - 7
SP  - 1005
EP  - 1013
PB  - Wiley-Blackwell
CY  - Oxford
ER  -