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Cathelicidin LL-37

Ein zentraler Faktor in der Pathogenese entzündlicher Dermatosen?

Cathelicidin LL-37

A central factor in the pathogenesis of inflammatory dermatoses?

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Zusammenfassung

Keratinozyten produzieren und sezernieren antimikrobielle Peptide, die innerhalb der angeborenen Immunabwehr der Haut wie endogene Antibiotika und wie Signalmoleküle wirken. Aktuelle Studien belegen, dass das antimikrobielle Peptid Cathelicidin LL-37 eine wichtige Rolle in der Pathogenese des atopischen Ekzems, der Rosazea und der Psoriasis spielt. Während eine verminderte Expression von Cathelicidin an der Hautoberfläche von Patienten mit atopischem Ekzem zu einer gesteigerten Anfälligkeit für Superinfektionen beiträgt, führt die Überexpression von Cathelicidinbruchstücken zur Entzündung bei der Rosazea. Schließlich konnte aktuell gezeigt werden, dass Cathelicidinpeptid, gekoppelt an körpereigene DNA, eine Autoimmunantwort in der Psoriasis auslöst. Diese Studien charakterisieren Cathelicidin als einen zentralen Faktor in der Pathogenese entzündlicher Dermatosen. Neue Behandlungsmethoden, die auf die Expression und Funktion von Cathelicidin abzielen, könnten deshalb das Spektrum der bislang eingesetzten Therapien erweitern.

Abstract

Keratinocytes produce and secrete antimicrobial peptides which function as endogenous antibiotics and as signaling molecules within the cutaneous innate immune system. Recent studies demonstrate that the antimicrobial peptide cathelicidin LL-37 plays an important role in the pathogenesis of atopic eczema, rosacea and psoriasis. Whereas skin in atopic eczema shows decreased cathelicidin expression which leads to increased susceptibility to superinfection in those patients, overabundant expression of cathelicidin peptide fragments causes inflammation in rosacea. Finally, in psoriasis cathelicidin peptide binds to self DNA which triggers an autoimmune response. These studies demonstrate the role of cathelicidin as a central factor in the pathogenesis of cutaneous inflammation. Therapies targeting cathelicidin expression and function could lead to new treatments for these diseases.

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Literatur

  1. Agerberth B, Charo J, Werr J et al. (2000) The human antimicrobial and chemotactic peptides LL-37 and alpha-defensins are expressed by specific lymphocyte and monocyte populations. Blood 96: 3086–3093

    PubMed  CAS  Google Scholar 

  2. Braff MH, Hawkins MA, Di Nardo A et al. (2005) Structure-function relationships among human cathelicidin peptides: dissociation of antimicrobial properties from host immunostimulatory activities. J Immunol 174: 4271–4278

    PubMed  CAS  Google Scholar 

  3. Dorschner RA, Pestonjamasp VK, Tamakuwala S et al. (2001) Cutaneous injury induces the release of cathelicidin anti-microbial peptides active against group A Streptococcus. J Invest Dermatol 117: 91–97

    Article  PubMed  CAS  Google Scholar 

  4. Howell MD, Gallo RL, Boguniewicz M et al. (2006) Cytokine milieu of atopic dermatitis skin subverts the innate immune response to vaccinia virus. Immunity 24: 341–348

    Article  PubMed  CAS  Google Scholar 

  5. Koczulla R, von Degenfeld G, Kupatt C et al. (2003) An angiogenic role for the human peptide antibiotic LL-37/hCAP-18. J Clin Invest 111: 1665–1672

    Article  PubMed  CAS  Google Scholar 

  6. Lande R, Gregorio J, Facchinetti V et al. (2007) Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide. Nature 449: 564–569

    Article  PubMed  CAS  Google Scholar 

  7. Nomura I, Goleva E, Howell MD et al. (2003) Cytokine milieu of atopic dermatitis, as compared to psoriasis, skin prevents induction of innate immune response genes. J Immunol 171: 3262–3269

    PubMed  CAS  Google Scholar 

  8. Ong PY, Ohtake T, Brandt C et al. (2002) Endogenous antimicrobial peptides and skin infections in atopic dermatitis. N Engl J Med 347: 1151–1160

    Article  PubMed  CAS  Google Scholar 

  9. Schauber J, Dorschner RA, Coda AB et al. (2007) Injury enhances TLR2 function and antimicrobial peptide expression through a vitamin D-dependent mechanism. J Clin Invest 117: 803–811

    Article  PubMed  CAS  Google Scholar 

  10. Yamasaki K, Di Nardo A, Bardan A et al. (2007) Increased serine protease activity and cathelicidin promotes skin inflammation in rosacea. Nat Med 13: 975–980

    Article  PubMed  CAS  Google Scholar 

  11. Yamasaki K, Schauber J, Coda A et al. (2006) Kallikrein-mediated proteolysis regulates the antimicrobial effects of cathelicidins in skin. Faseb J 20: 2068–2080

    Article  PubMed  CAS  Google Scholar 

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Correspondence to J. Schauber.

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Schauber, J., Ruzicka, T. & Rupec, R. Cathelicidin LL-37. Hautarzt 59, 72–74 (2008). https://doi.org/10.1007/s00105-007-1457-z

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