Statins inhibit chemotactic interaction between CCL20 and CCR6 in vitro: Possible relevance to psoriasis treatment

Tae Gyun Kim, Dashlkhumbe Byamba, Wen Hao Wu, Min Geol Lee

Research output: Contribution to journalLetter

15 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)855-857
Number of pages3
JournalExperimental dermatology
Volume20
Issue number10
DOIs
Publication statusPublished - 2011 Oct 1

Fingerprint

fluvastatin
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Psoriasis
Simvastatin
T-cells
Interleukin-23
T-Lymphocytes
Th17 Cells
Pravastatin
Interleukin-17
Chemotaxis
Interleukin-1
Keratinocytes
Infiltration
Skin Diseases
Assays
Skin
Therapeutics
Cytokines
Lipids

All Science Journal Classification (ASJC) codes

  • Dermatology
  • Molecular Biology
  • Biochemistry

Cite this

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title = "Statins inhibit chemotactic interaction between CCL20 and CCR6 in vitro: Possible relevance to psoriasis treatment",
abstract = "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.",
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Statins inhibit chemotactic interaction between CCL20 and CCR6 in vitro : Possible relevance to psoriasis treatment. / Kim, Tae Gyun; Byamba, Dashlkhumbe; Wu, Wen Hao; Lee, Min Geol.

In: Experimental dermatology, Vol. 20, No. 10, 01.10.2011, p. 855-857.

Research output: Contribution to journalLetter

TY - JOUR

T1 - Statins inhibit chemotactic interaction between CCL20 and CCR6 in vitro

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AU - Kim, Tae Gyun

AU - Byamba, Dashlkhumbe

AU - Wu, Wen Hao

AU - Lee, Min Geol

PY - 2011/10/1

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N2 - 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.

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