PMID- 21716128
OWN - NLM
STAT- MEDLINE
DCOM- 20120325
LR  - 20171116
IS  - 1708-8267 (Electronic)
IS  - 1081-5589 (Linking)
VI  - 59
IP  - 7
DP  - 2011 Oct
TI  - Prostaglandin I2 analogs suppress tumor necrosis factor alpha production and the 
      maturation of human monocyte-derived dendritic cells.
PG  - 1109-15
LID - 10.2310/JIM.0b013e3182281f62 [doi]
AB  - BACKGROUND: Dendritic cells (DCs) are professional antigen-presenting cells and 
      have critical roles in regulating immune responses. Prostaglandin I2 (PGI2) 
      analogs are considered to be potential treatments for asthma. However, the effect 
      of PGI2 analogs on human monocyte-derived DCs (MDDCs) is still not clearly 
      understood. METHODS: Human MDDCs were pretreated with iloprost and treprostinil 
      (2 PGI2 analogs) or forskolin (an adenyl cyclase activator) before 
      lipopolysaccharide (LPS) stimulation. In some cases, I prostanoid (IP) receptor 
      and E prostanoid receptor antagonists were added before the PGI2 analog 
      treatment. tumor necrosis factor alpha (TNF-alpha) was measured by enzyme-linked 
      immunosorbent assay. The expression of costimulatory molecules was assessed by 
      flow cytometry. T-cell polarization function was investigated by measuring 
      interferon gamma, interleukin 13 (IL-13), and IL-17A production by T cells cocultured 
      with iloprost-treated MDDCs. RESULTS: Iloprost and treprostinil suppressed 
      LPS-induced TNF-alpha expression in MDDCs. This effect could be reversed by an IP 
      receptor antagonist, CAY10449, but not by E prostanoid receptor antagonists. 
      Forskolin conferred a similar effect. Iloprost suppressed the LPS-induced 
      expression of costimulatory molecules, including CD80, CD86, CD40, and HLA-DR. 
      Iloprost-treated MDDCs increased IL-17A production by T cells. CONCLUSIONS: 
      Prostaglandin I2 analogs may exert anti-inflammatory effects by suppressing TNF-alpha 
      expression via the IP receptor-cyclic adenosine monophosphate pathways and by 
      inhibiting the expression of costimulatory molecules in human MDDCs.
FAU - Yeh, Ching-Hui
AU  - Yeh CH
AD  - Department of Family Medicine, Zuoying Armed Force General Hospital, Kaohsiung, 
      Taiwan.
FAU - Kuo, Chang-Hung
AU  - Kuo CH
FAU - Yang, San-Nan
AU  - Yang SN
FAU - Huang, Ming-Yii
AU  - Huang MY
FAU - Wu, Hsaing-Chi
AU  - Wu HC
FAU - Wang, Hsing-Pi
AU  - Wang HP
FAU - Kuo, Thai-Hung
AU  - Kuo TH
FAU - Hung, Chih-Hsing
AU  - Hung CH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Investig Med
JT  - Journal of investigative medicine : the official publication of the American 
      Federation for Clinical Research
JID - 9501229
RN  - 0 (Benzophenones)
RN  - 0 (CAY10449)
RN  - 0 (Imidazoles)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (PTGER1 protein, human)
RN  - 0 (Receptors, Prostaglandin E, EP1 Subtype)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Vasodilator Agents)
RN  - DCR9Z582X0 (Epoprostenol)
RN  - E0399OZS9N (Cyclic AMP)
RN  - JED5K35YGL (Iloprost)
RN  - RUM6K67ESG (treprostinil)
SB  - IM
MH  - Asthma/drug therapy/metabolism
MH  - Benzophenones/chemistry/*pharmacology
MH  - Cyclic AMP/metabolism
MH  - Dendritic Cells/*cytology
MH  - Epoprostenol/*analogs & derivatives/pharmacology
MH  - Humans
MH  - Iloprost/pharmacology
MH  - Imidazoles/chemistry/*pharmacology
MH  - Immune System
MH  - Leukocytes, Mononuclear/cytology
MH  - Lipopolysaccharides/metabolism
MH  - Monocytes/*cytology
MH  - Receptors, Prostaglandin E, EP1 Subtype/antagonists & inhibitors
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
MH  - Vasodilator Agents/pharmacology
EDAT- 2011/07/01 06:00
MHDA- 2012/03/27 06:00
CRDT- 2011/07/01 06:00
PHST- 2011/07/01 06:00 [entrez]
PHST- 2011/07/01 06:00 [pubmed]
PHST- 2012/03/27 06:00 [medline]
AID - 10.2310/JIM.0b013e3182281f62 [doi]
PST - ppublish
SO  - J Investig Med. 2011 Oct;59(7):1109-15. doi: 10.2310/JIM.0b013e3182281f62.