Cathelicidin Antimicrobial Peptide LL-37 in Psoriasis Enables Keratinocyte Reactivity against TLR9 Ligands

Here we show that keratinocytes in psoriatic lesional skin express increased Toll-like receptor (TLR) 9 that similarly localizes with elevated expression of the cathelicidin antimicrobial peptide LL-37. In culture, normal human keratinocytes exposed to LL-37 increased TLR9 expression. Furthermore, w...

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Published in	Journal of investigative dermatology Vol. 132; no. 1; pp. 135 - 143
Main Authors	Morizane, Shin, Yamasaki, Kenshi, Mühleisen, Beda, Kotol, Paul F., Murakami, Masamoto, Aoyama, Yumi, Iwatsuki, Keiji, Hata, Tissa, Gallo, Richard L.
Format	Journal Article
Language	English
Published	New York, NY Elsevier Inc 01.01.2012 Nature Publishing Group Elsevier Limited
Subjects	Antimicrobial Cationic Peptides Biological and medical sciences Biopsy Cathelicidins - genetics Cathelicidins - immunology Cathelicidins - metabolism Cells, Cultured CpG Islands - genetics CpG Islands - immunology Dermatology DNA - immunology DNA - pharmacology Epidermal Cells Gene Expression - immunology Humans Interferon Type I - genetics Interferon Type I - immunology Interferon Type I - metabolism Interferon-beta - genetics Interferon-beta - immunology Interferon-beta - metabolism Keratinocytes - cytology Keratinocytes - physiology Ligands Medical sciences Psoriasis - immunology Psoriasis - physiopathology Psoriasis. Parapsoriasis. Lichen Toll-Like Receptor 9 - immunology Toll-Like Receptor 9 - metabolism Skin disease Peptides Psoriasis Dermatology Ligand Keratinocyte Antimicrobial agent
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Abstract	Here we show that keratinocytes in psoriatic lesional skin express increased Toll-like receptor (TLR) 9 that similarly localizes with elevated expression of the cathelicidin antimicrobial peptide LL-37. In culture, normal human keratinocytes exposed to LL-37 increased TLR9 expression. Furthermore, when keratinocytes were exposed to LL-37 and subsequently treated with TLR9 ligands, such as CpG or genomic DNA, they greatly increased production of type I IFNs. This response mimicked observations in the epidermis of psoriatic lesional skin as keratinocytes in psoriatic lesions produce greater amounts of IFN-β than normal skin lacking LL-37. The mechanism for induction of type I IFNs in keratinocytes was dependent on TLR9 expression but not on a DNA–LL-37 complex. These findings suggest that keratinocytes recognize and respond to DNA and can actively participate in contributing to the immunological environment that characterizes psoriasis.
AbstractList	Here we show that keratinocytes in psoriatic lesional skin express increased Toll-like receptor (TLR) 9 that similarly localizes with elevated expression of the cathelicidin antimicrobial peptide LL-37. In culture, normal human keratinocytes exposed to LL-37 increased TLR9 expression. Furthermore, when keratinocytes were exposed to LL-37 and subsequently treated with TLR9 ligands, such as CpG or genomic DNA, they greatly increased production of type I IFNs. This response mimicked observations in the epidermis of psoriatic lesional skin as keratinocytes in psoriatic lesions produce greater amounts of IFN-[beta] than normal skin lacking LL-37. The mechanism for induction of type I IFNs in keratinocytes was dependent on TLR9 expression but not on a DNA-LL-37 complex. These findings suggest that keratinocytes recognize and respond to DNA and can actively participate in contributing to the immunological environment that characterizes psoriasis. Here we show that keratinocytes in psoriatic lesional skin express increased Toll-like receptor (TLR) 9 that similarly localizes with elevated expression of the cathelicidin antimicrobial peptide LL-37. In culture, normal human keratinocytes exposed to LL-37 increased TLR9 expression. Furthermore, when keratinocytes were exposed to LL-37 and subsequently treated with TLR9 ligands, such as CpG or genomic DNA, they greatly increased production of type I IFNs. This response mimicked observations in the epidermis of psoriatic lesional skin as keratinocytes in psoriatic lesions produce greater amounts of IFN-β than normal skin lacking LL-37. The mechanism for induction of type I IFNs in keratinocytes was dependent on TLR9 expression but not on a DNA–LL-37 complex. These findings suggest that keratinocytes recognize and respond to DNA and can actively participate in contributing to the immunological environment that characterizes psoriasis. Here we show that keratinocytes in psoriatic lesional skin express increased Toll-like receptor (TLR) 9 that similarly localizes with elevated expression of the cathelicidin antimicrobial peptide LL-37. In culture, normal human keratinocytes exposed to LL-37 increased TLR9 expression. Furthermore, when keratinocytes were exposed to LL-37 and subsequently treated with TLR9 ligands such as CpG or genomic DNA, keratinocytes greatly increased production of type I interferons. This response mimicked observations in the epidermis of psoriatic lesional skin as keratinocytes in psoriatic lesions produce greater amounts of interferon-β than normal skin lacking LL-37. The mechanism for induction of type I interferons in keratinocytes was dependent on TLR9 expression but not on a DNA-LL-37 complex. These findings suggest that keratinocytes recognize and respond to DNA and can actively participate in contributing to the immunological environment that characterizes psoriasis.
Author	Aoyama, Yumi Gallo, Richard L. Morizane, Shin Iwatsuki, Keiji Mühleisen, Beda Hata, Tissa Yamasaki, Kenshi Murakami, Masamoto Kotol, Paul F.
AuthorAffiliation	1 Division of Dermatology, Department of Medicine, University of California, San Diego and VA San Diego Healthcare System, San Diego, CA, USA 3 Department of Dermatology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan 4 Department of Dermatology, Asahikawa Medical College, Asahikawa, Japan 2 Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan
AuthorAffiliation_xml	– name: 1 Division of Dermatology, Department of Medicine, University of California, San Diego and VA San Diego Healthcare System, San Diego, CA, USA – name: 4 Department of Dermatology, Asahikawa Medical College, Asahikawa, Japan – name: 2 Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan – name: 3 Department of Dermatology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan
Author_xml	– sequence: 1 givenname: Shin surname: Morizane fullname: Morizane, Shin email: zanemori@cc.okayama-u.ac.jp organization: Division of Dermatology, Department of Medicine, University of California, San Diego and VA San Diego Healthcare System, San Diego, California, USA – sequence: 2 givenname: Kenshi surname: Yamasaki fullname: Yamasaki, Kenshi organization: Division of Dermatology, Department of Medicine, University of California, San Diego and VA San Diego Healthcare System, San Diego, California, USA – sequence: 3 givenname: Beda surname: Mühleisen fullname: Mühleisen, Beda organization: Division of Dermatology, Department of Medicine, University of California, San Diego and VA San Diego Healthcare System, San Diego, California, USA – sequence: 4 givenname: Paul F. surname: Kotol fullname: Kotol, Paul F. organization: Division of Dermatology, Department of Medicine, University of California, San Diego and VA San Diego Healthcare System, San Diego, California, USA – sequence: 5 givenname: Masamoto surname: Murakami fullname: Murakami, Masamoto organization: Department of Dermatology, Asahikawa Medical College, Asahikawa, Japan – sequence: 6 givenname: Yumi surname: Aoyama fullname: Aoyama, Yumi organization: Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan – sequence: 7 givenname: Keiji surname: Iwatsuki fullname: Iwatsuki, Keiji organization: Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan – sequence: 8 givenname: Tissa surname: Hata fullname: Hata, Tissa organization: Division of Dermatology, Department of Medicine, University of California, San Diego and VA San Diego Healthcare System, San Diego, California, USA – sequence: 9 givenname: Richard L. surname: Gallo fullname: Gallo, Richard L. organization: Division of Dermatology, Department of Medicine, University of California, San Diego and VA San Diego Healthcare System, San Diego, California, USA
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References	Braff, Hawkins, Di Nardo (bb0010) 2005; 174 Gallo, Ono, Povsic (bb0045) 1994; 91 Nestle, Conrad, Tun-Kyi (bb0100) 2005; 202 Harder, Bartels, Christophers (bb0055) 1997; 387 Liu, Wang, Jia (bb0075) 1998; 222 Morizane, Yamasaki, Kabigting (bb0090) 2010; 130 Lande, Gregorio, Facchinetti (bb0065) 2007; 449 Nestle, Kaplan, Barker (bb0105) 2009; 361 Di Cesare, Di Meglio, Nestle (bb0020) 2009; 129 Lai, Gallo (bb0060) 2009; 30 Ganguly, Chamilos, Lande (bb0050) 2009; 206 Frohm, Agerberth, Ahangari (bb0040) 1997; 272 Dombrowski, Peric, Koglin (bb0030) 2011; 3 Taylor, Yamasaki, Radek (bb0115) 2007; 282 Di Nardo, Braff, Taylor (bb0025) 2007; 178 Miller, Sorensen, Liu (bb0085) 2005; 174 Buchau, MacLeod, Morizane (bb0015) 2009; 129 Yamasaki, Di Nardo, Bardan (bb0120) 2007; 13 Lebre, van der Aar, van Baarsen (bb0070) 2007; 127 Miller, Hata, Kotol (bb0080) 2011; 131 Dorschner, Pestonjamasp, Tamakuwala (bb0035) 2001; 117 Murakami, Lopez-Garcia, Braff (bb0095) 2004; 172 Ong, Ohtake, Brandt (bb0110) 2002; 347 Lebre, MC, van der Aar, AM, van Baarsen, L 2007; 127 Buchau, AS, MacLeod, DT, Morizane, S 2009; 129 Dombrowski, Y, Peric, M, Koglin, S 2011; 3 Braff, MH, Hawkins, MA, Di Nardo, A 2005; 174 Taylor, KR, Yamasaki, K, Radek, KA 2007; 282 Morizane, S, Yamasaki, K, Kabigting, FD 2010; 130 Gallo, RL, Ono, M, Povsic, T 1994; 91 Lande, R, Gregorio, J, Facchinetti, V 2007; 449 Nestle, FO, Conrad, C, Tun-Kyi, A 2005; 202 Miller, J, Hata, T, Kotol, PF 2011; 131 Yamasaki, K, Di Nardo, A, Bardan, A 2007; 13 Lai, Y, Gallo, RL 2009; 30 Nestle, FO, Kaplan, DH, Barker, J 2009; 361 Frohm, M, Agerberth, B, Ahangari, G 1997; 272 Ganguly, D, Chamilos, G, Lande, R 2009; 206 Ong, PY, Ohtake, T, Brandt, C 2002; 347 Harder, J, Bartels, J, Christophers, E 1997; 387 Dorschner, RA, Pestonjamasp, VK, Tamakuwala, S 2001; 117 Liu, L, Wang, L, Jia, HP 1998; 222 Di Cesare, A, Di Meglio, P, Nestle, FO 2009; 129 Miller, LS, Sorensen, OE, Liu, PT 2005; 174 Di Nardo, A, Braff, MH, Taylor, KR 2007; 178 Murakami, M, Lopez-Garcia, B, Braff, M 2004; 172 Buchau (10.1038/jid.2011.259_bb0015) 2009; 129 Taylor (10.1038/jid.2011.259_bb0115) 2007; 282 Braff (10.1038/jid.2011.259_bb0010) 2005; 174 Di Cesare (10.1038/jid.2011.259_bb0020) 2009; 129 Frohm (10.1038/jid.2011.259_bb0040) 1997; 272 Nestle (10.1038/jid.2011.259_bb0105) 2009; 361 Ganguly (10.1038/jid.2011.259_bb0050) 2009; 206 Nestle (10.1038/jid.2011.259_bb0100) 2005; 202 Harder (10.1038/jid.2011.259_bb0055) 1997; 387 Lande (10.1038/jid.2011.259_bb0065) 2007; 449 Dombrowski (10.1038/jid.2011.259_bb0030) 2011; 3 Gallo (10.1038/jid.2011.259_bb0045) 1994; 91 Liu (10.1038/jid.2011.259_bb0075) 1998; 222 Miller (10.1038/jid.2011.259_bb0080) 2011; 131 Di Nardo (10.1038/jid.2011.259_bb0025) 2007; 178 Yamasaki (10.1038/jid.2011.259_bb0120) 2007; 13 Morizane (10.1038/jid.2011.259_bb0090) 2010; 130 Dorschner (10.1038/jid.2011.259_bb0035) 2001; 117 Murakami (10.1038/jid.2011.259_bb0095) 2004; 172 Miller (10.1038/jid.2011.259_bb0085) 2005; 174 Lebre (10.1038/jid.2011.259_bb0070) 2007; 127 Ong (10.1038/jid.2011.259_bb0110) 2002; 347 Lai (10.1038/jid.2011.259_bb0060) 2009; 30
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Snippet	Here we show that keratinocytes in psoriatic lesional skin express increased Toll-like receptor (TLR) 9 that similarly localizes with elevated expression of...
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SubjectTerms	Antimicrobial Cationic Peptides Biological and medical sciences Biopsy Cathelicidins - genetics Cathelicidins - immunology Cathelicidins - metabolism Cells, Cultured CpG Islands - genetics CpG Islands - immunology Dermatology DNA - immunology DNA - pharmacology Epidermal Cells Gene Expression - immunology Humans Interferon Type I - genetics Interferon Type I - immunology Interferon Type I - metabolism Interferon-beta - genetics Interferon-beta - immunology Interferon-beta - metabolism Keratinocytes - cytology Keratinocytes - physiology Ligands Medical sciences Psoriasis - immunology Psoriasis - physiopathology Psoriasis. Parapsoriasis. Lichen Toll-Like Receptor 9 - immunology Toll-Like Receptor 9 - metabolism
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Title	Cathelicidin Antimicrobial Peptide LL-37 in Psoriasis Enables Keratinocyte Reactivity against TLR9 Ligands
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