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Statins inhibit chemotactic interaction between CCL20 and CCR6 in vitro : possible relevance to psoriasis treatment
Author(s) -
Kim TaeGyun,
Byamba Dashlkhumbe,
Wu Wen Hao,
Lee MinGeol
Publication year - 2011
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2011.01343.x
Subject(s) - ccl20 , c c chemokine receptor type 6 , simvastatin , psoriasis , fluvastatin , chemistry , chemotaxis , cytokine , pharmacology , statin , immune system , immunology , chemokine , cancer research , medicine , biochemistry , receptor , chemokine receptor
Psoriasis is a chronic IL‐23/Th17 pathway‐associated skin disease. An increased expression of lesional CCL20 can recruit CCR6+ Th17, and lesional cytokine milieu persistently activates keratinocytes to produce CCL20. Lipid‐lowering drugs, statins, are known to possess immune‐modulating functions. In this study, we explored an inhibitory effect of statins on CCL20/CCR6 interaction. We demonstrated that IL‐1β, TNF‐α, and IL‐17A significantly increased CCL20 production from HaCaT cells. However, these increments were markedly inhibited by fluvastatin and simvastatin, but not by pravastatin. In the chemotaxis migration assay, pretreatment with fluvastatin and simvastatin inhibited the migration of human CD4+ T cells towards CCL20. However, the level of CCR6 surface expression in memory CD4+ T cells was not affected. Our results suggest that not all, but specific types of statins may be of benefit in alleviating psoriasis partially via interrupting CCL20/CCR6 chemotactic interaction, the mechanism which may eventually lessen the infiltration of Th17 cells.