Source:http://linkedlifedata.com/resource/pubmed/id/16428071
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2006-1-23
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pubmed:abstractText |
Topical immunosuppressant therapy is widely used in the treatment of inflammatory skin diseases such as psoriasis and atopic dermatitis. Besides its beneficial therapeutic effects, application of topical anti-inflammatory drugs may render the epidermis more vulnerable to invading pathogens by suppressing innate immune responses in keratinocytes, such as cytokine production and Toll-like receptor (TLR) expression. In order to evaluate and compare the immunosuppressive effects of different immunosuppressant drugs on keratinocytes, we treated lipopolysaccharide (LPS)-stimulated and -unstimulated normal human keratinocytes with the synthetic corticosteroid budesonide and the macrolide tacrolimus. The expressions of the pattern recognition receptors (PRRs) TLR2 and TLR4 were measured by quantitative RT-PCR, pro-inflammatory cytokines IL-1alpha, IL-8 and TNF-alpha were monitored by quantitative RT-PCR and by ELISA, and alterations in TLR2 protein level were measured by flow cytometry. Budesonide had a suppressive effect on both constitutive and LPS-induced IL-8 gene expression. The amount of TNF-alpha mRNA was diminished in unstimulated keratinocytes, while TLR2 mRNA expression was markedly enhanced both in unstimulated and LPS-treated cells after incubation with budesonide. This increase in TLR2 mRNA expression was also detectable at the protein level in LPS-stimulated cells. Tacrolimus had no effect on any of the examined genes. Budesonide, but not tacrolimus, significantly inhibited the NF-kappaB-dependent luciferase reporter activity in HaCaT cells after induction with LPS or TNF-alpha. Although tacrolimus and budesonide are both effective treatments in some inflammatory skin diseases, the data provided here imply differences in local therapeutic and adverse effects of these two topical immunosuppressants.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Budesonide,
http://linkedlifedata.com/resource/pubmed/chemical/Immunosuppressive Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/TLR2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Tacrolimus,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 2,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1567-5769
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
358-68
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pubmed:meshHeading |
pubmed-meshheading:16428071-Anti-Inflammatory Agents,
pubmed-meshheading:16428071-Budesonide,
pubmed-meshheading:16428071-Cell Line,
pubmed-meshheading:16428071-Cells, Cultured,
pubmed-meshheading:16428071-Gene Expression,
pubmed-meshheading:16428071-Genes, Reporter,
pubmed-meshheading:16428071-Humans,
pubmed-meshheading:16428071-Immunosuppressive Agents,
pubmed-meshheading:16428071-Interleukin-8,
pubmed-meshheading:16428071-Keratinocytes,
pubmed-meshheading:16428071-Lipopolysaccharides,
pubmed-meshheading:16428071-NF-kappa B,
pubmed-meshheading:16428071-RNA, Messenger,
pubmed-meshheading:16428071-Tacrolimus,
pubmed-meshheading:16428071-Toll-Like Receptor 2,
pubmed-meshheading:16428071-Tumor Necrosis Factor-alpha
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pubmed:year |
2006
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pubmed:articleTitle |
Budesonide, but not tacrolimus, affects the immune functions of normal human keratinocytes.
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pubmed:affiliation |
Department of Clinical Pharmacy, Faculty of Pharmacy, University of Szeged, Szeged, Hungary. kiskori@freemail.hu
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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