PMID- 11235021
OWN - NLM
STAT- MEDLINE
DCOM- 20010531
LR  - 20131121
IS  - 1023-3830 (Print)
IS  - 1023-3830 (Linking)
VI  - 50
IP  - 1
DP  - 2001 Jan
TI  - Dithranol upregulates IL-10 receptors on the cultured human keratinocyte cell 
      line HaCaT.
PG  - 44-9
AB  - OBJECTIVE: Dithranol is highly effective in the treatment of psoriasis, however 
      its mode of action is still not well known. Since interleukin-8 and 
      interleukin-10 are involved in the pathogenesis of psoriasis, the aim of our 
      study was to investigate the effect of dithranol on interleukin-8, interleukin-10 
      mRNA production and interleukin-10 receptor expression of the HaCaT keratinocyte 
      cell line which is commonly used in experiments examining the effects of 
      therapeutic drugs on keratinocytes. MATERIALS AND METHODS: Cultured HaCaT cells 
      were treated with 0.1-0.5 microg/ml dithranol for 30 minutes. After 2 and 4 h 
      total cellular RNA isolated from HaCaT cells was reverse transcribed (RT) to cDNA 
      which was subjected to polymerase chain reaction (PCR) with specific primer pairs 
      for interleukin-8, interleukin-10 and interleukin-10 receptor. For 
      immunohistochemistry cultured HaCaT cells were stained with a monoclonal antibody 
      against the human interleukin-10 receptor. RESULTS: Our results showed that 
      dithranol treatment did not change the highly elevated level of interleukin-8 
      mRNA of HaCaT cells. Interleukin-10 mRNA signal with RT-PCR could not be detected 
      in HaCaT cells. Depending on the concentration dithranol increased the mRNA 
      production of interleukin-10 receptors in HaCaT cells. This dithranol induced 
      dose dependent upregulation of IL-10 receptors in HaCaT cells was also observed 
      on the protein level using immunohistochemistry. CONCLUSIONS: Since the 
      interleukin-10 receptor expression of keratinocytes in psoriatic lesional skin is 
      downregulated, the dithranol induced upregulation of the receptor in our model 
      system might help to reveal the therapeutic action of the drug.
FAU - Farkas, A
AU  - Farkas A
AD  - Department of Dermatology, Faculty of General Medicine, University of Szeged, 
      Hungary. farkas@derma.szote.u-szeged.hu
FAU - Kemeny, L
AU  - Kemeny L
FAU - Szony, B J
AU  - Szony BJ
FAU - Bata-Csorgo, Z
AU  - Bata-Csorgo Z
FAU - Pivarcsi, A
AU  - Pivarcsi A
FAU - Kiss, M
AU  - Kiss M
FAU - Szell, M
AU  - Szell M
FAU - Koreck, A
AU  - Koreck A
FAU - Dobozy, A
AU  - Dobozy A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Inflamm Res
JT  - Inflammation research : official journal of the European Histamine Research 
      Society ... [et al.]
JID - 9508160
RN  - 0 (Actins)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Interleukin-8)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Interleukin)
RN  - 0 (Receptors, Interleukin-10)
RN  - 130068-27-8 (Interleukin-10)
RN  - U8CJK0JH5M (Anthralin)
SB  - IM
MH  - Actins/genetics
MH  - Administration, Topical
MH  - Anthralin/administration & dosage/*pharmacology
MH  - Anti-Inflammatory Agents/administration & dosage/*pharmacology
MH  - Antibodies, Monoclonal/pharmacology
MH  - Cell Line
MH  - Cell Line, Transformed
MH  - Cells, Cultured
MH  - Gene Expression Regulation/*drug effects
MH  - Humans
MH  - Immunohistochemistry
MH  - Interleukin-10/genetics
MH  - Interleukin-8/genetics
MH  - Keratinocytes/*metabolism
MH  - RNA, Messenger/analysis
MH  - Receptors, Interleukin/*genetics/immunology
MH  - Receptors, Interleukin-10
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2001/03/10 10:00
MHDA- 2001/06/02 10:01
CRDT- 2001/03/10 10:00
PHST- 2001/03/10 10:00 [pubmed]
PHST- 2001/06/02 10:01 [medline]
PHST- 2001/03/10 10:00 [entrez]
AID - 10.1007/s000110050723 [pii]
AID - 10.1007/s000110050723 [doi]
PST - ppublish
SO  - Inflamm Res. 2001 Jan;50(1):44-9. doi: 10.1007/s000110050723.