Document Detail


KdPT, a tripeptide derivative of alpha-melanocyte-stimulating hormone, suppresses IL-1 beta-mediated cytokine expression and signaling in human sebocytes.
MedLine Citation:
PMID:  20610647     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Acne is the most common inflammatory skin disease in which IL-1 plays a central role. Although alpha-melanocyte-stimulating hormone has immunomodulatory effects, its usefulness as an anti-inflammatory agent in acne is hampered owing to its lipid- and pigment-inducing effects via activation of melanocortin receptors (MC-Rs). We used the immortalized human sebocyte line SZ95 as an in vitro model to investigate the anti-inflammatory potential of KdPT, a tripeptide derivative of the C-terminal end of alpha-melanocyte-stimulating hormone. KdPT potently suppressed IL-1beta-induced IL-6 and IL-8 expression. Mechanistically, KdPT decreased IL-1beta-mediated IkappaBalpha degradation, reduced nuclear accumulation of p65, and attenuated DNA binding of NF-kappaB. Moreover, KdPT reduced IL-1beta-mediated generation of intracellular reactive oxygen species, which contributed to IL-1beta-mediated cytokine induction. KdPT also reduced cell surface binding of fluorochrome-labeled IL-1beta in SZ95 sebocytes. Analysis of the crystal structure of the complex between IL-1beta/IL-1R type I (IL-1RI), followed by computer modeling of KdPT and subsequent modeling of the peptide receptor complex with the crystal structure of IL-1RI via manual docking, further predicted that the tripeptide, through several H-bonds and one hydrophobic bond, interacts with the IL-1RI. Importantly, KdPT did not bind to MC-1Rs, as demonstrated by blocking experiments with a peptide analog of Agouti signaling protein and by binding assays using MC-1R-expressing B16 melanoma cells. Accordingly, KdPT failed to induce melanogenesis. Our data demonstrate a promising anti-inflammatory potential of KdPT and point toward novel future directions in the treatment of acne-as well as of various other IL-1-mediated inflammatory diseases-with this small molecule.
Authors:
Arianna Mastrofrancesco; Agatha Kokot; Alex Eberle; Nicholas C J Gibbons; Karin U Schallreuter; Elwira Strozyk; Mauro Picardo; Christos C Zouboulis; Thomas A Luger; Markus Böhm
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-07-07
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  185     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-27     Completed Date:  2010-09-08     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1903-11     Citation Subset:  AIM; IM    
Affiliation:
Department of Dermatology, University of Münster, Münster, Germany.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Line
Cell Line, Transformed
Cytokines / antagonists & inhibitors*,  biosynthesis
DNA-Binding Proteins / physiology
Humans
I-kappa B Kinase / antagonists & inhibitors,  metabolism
I-kappa B Proteins / antagonists & inhibitors,  metabolism
Immunosuppressive Agents / pharmacology*
Interleukin-1beta / antagonists & inhibitors*,  physiology
Interleukin-6 / antagonists & inhibitors
Interleukin-8 / antagonists & inhibitors
Melanoma, Experimental
Mice
Peptide Fragments / physiology*
Sebaceous Glands / cytology*,  immunology*,  metabolism
Signal Transduction / immunology*
alpha-MSH / physiology*
Chemical
Reg. No./Substance:
0/Cytokines; 0/DNA-Binding Proteins; 0/I-kappa B Proteins; 0/Immunosuppressive Agents; 0/Interleukin-1beta; 0/Interleukin-6; 0/Interleukin-8; 0/Peptide Fragments; 117027-34-6/interleukin 1beta (193-195); 139874-52-5/NF-kappaB inhibitor alpha; 581-05-5/alpha-MSH; EC 2.7.11.10/I-kappa B Kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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