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ID 53018
フルテキストURL
著者
Takiguchi, T Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci
Morizane, S Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci 科研費研究者番号
Yamamoto, T Kawasaki Med Univ, Dept Dermatol
Kajita, A Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci
Ikeda, K Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci
Iwatsuki, K Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci
抄録
Background Cathelicidin antimicrobial peptide LL-37 has the capacity to kill a wide range of microbes and to modify host immunity. Recently, our group observed that the activation of keratinocytes by LL-37 and DNA greatly increases interferon (IFN)-beta through Toll-like receptor (TLR) 9. However, the effect of LL-37 on the induction of IFN-beta through TLR3, a sensor of double-stranded (ds) RNA, in keratinocytes is not well known. Objectives To investigate whether LL-37 could affect TLR3 signalling and antiviral activity in normal human epidermal keratinocytes (NHEKs). Methods We investigated the production of IFN-beta in NHEKs stimulated with a TLR3 ligand, poly (I:C), in the presence of LL-37. To examine the effect of LL-37 and poly (I:C) on antiviral activity, a virus plaque assay using herpes simplex (HS) virus type-1 was carried out. The uptake of poly (I:C) conjugated with fluorescein isothiocyanate (FITC) into the keratinocytes was observed in the presence of LL-37. Immunostaining for TLR3 and LL-37 was performed using skin samples from HS. Results LL-37 and poly (I:C) synergistically induced the expression of IFN-beta in NHEKs. Furthermore, co-stimulation with LL-37 and poly (I:C) significantly decreased the viral plaque numbers compared with poly (I:C) or LL-37 alone. LL-37 enhanced the uptake of FITC-conjugated poly (I:C) into cells. Immunohistochemical analysis demonstrated that the expression of TLR3 and LL-37 is up-regulated in HS lesions. Conclusions Our findings suggest that LL-37 augments the antiviral activity induced by dsRNA in keratinocytes, which may contribute to the innate immune response to cutaneous viral infections such as HS.
備考
This is the accepted version of the following article: FULLCITE, which has been published in final form at http://dx.doi.org/10.1111/bjd.12942
学位審査副論文
発行日
2014-09
出版物タイトル
British Journal of Dermatology
171巻
3号
開始ページ
492
終了ページ
498
ISSN
0007-0963
資料タイプ
学術雑誌論文
言語
English
OAI-PMH Set
岡山大学
著作権者
© 2014 British Association of Dermatologists
論文のバージョン
author
PubMed ID
DOI
Web of Sience KeyUT
関連URL
http://ousar.lib.okayama-u.ac.jp/metadata/52974
http://ousar.lib.okayama-u.ac.jp/53764