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Involvement of adenosine triphosphate‐binding cassette subfamily B member 1 in the augmentation of triacylglycerol excretion by Propionibacterium acnes in differentiated hamster sebocytes
Author(s) -
Mizuno Koji,
Akimoto Noriko,
Kawamura Mina,
Nakase Keisuke,
Noguchi Norihisa,
Sato Takashi
Publication year - 2017
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/1346-8138.13963
Subject(s) - propionibacterium acnes , atp binding cassette transporter , secretion , acne , pharmacology , hamster , biology , extracellular , biochemistry , chemistry , medicine , transporter , endocrinology , gene , genetics
An onset of acne, a common inflammatory skin disease, is associated with excess sebum production and secretion in sebaceous glands. Because Propionibacterium acnes has been reported to augment intracellular sebum accumulation in sebaceous glands in hamsters, it remains unclear whether P. acnes influences sebum secretion from differentiated sebocytes. Both P. acnes culture media (Acnes73‐ CM ) and formalin‐killed P. acnes (F‐Acnes73) dose‐dependently increased the extracellular levels of triacylglycerol ( TG ), a major sebum component, and Rhodamine 123, a substrate of adenosine triphosphate‐binding cassette ( ABC ) transporter, from differentiated hamster sebocytes ( DHS ). In addition, the gene expression of the ABC subfamily B member 1 ( ABCB 1) was dose‐dependently augmented by adding Acnes73‐ CM and F‐Acnes73 into DHS . Furthermore, the F‐Acnes73‐induced increase of TG excretion was suppressed by PSC 833, a selective ABCB 1 inhibitor. On the other hand, peptidoglycan ( PGN ), which is a Toll‐like receptor 2 ( TLR 2) ligand in P. acnes , increased extracellular TG levels, transporter activity and ABCB 1 mRNA expression in DHS . The PGN ‐augmented TG excretion was suppressed by PSC 833. Thus, these results provide novel evidence that P. acnes facilitates sebum secretion due to the activation of ABCB 1 concomitantly with the increased ABCB 1 expression, which may result from the activation of the TLR 2 pathway in DHS . Therefore, the ABCB 1 inhibitor is likely to become a candidate as a possible therapeutic for the treatment of acne.