PMID- 15676206
OWN - NLM
STAT- MEDLINE
DCOM- 20050411
LR  - 20161124
IS  - 0301-472X (Print)
IS  - 0301-472X (Linking)
VI  - 33
IP  - 2
DP  - 2005 Feb
TI  - The cyclopentenone prostaglandin PGA2 costimulates the maturation of human 
      dendritic cells.
PG  - 144-50
AB  - OBJECTIVE: Dendritic cells (DCs), also referred to as the sentinels of the immune 
      system, induce and coordinate important functions of immune surveillance. 
      Prostaglandin E2 (PGE2), a member of the eicosanoid family of arachidonic acid 
      derivatives, is widely used to enhance the TNF-alpha-driven maturation of human 
      monocyte-derived DCs (moDCs) both in basic research and in clinical settings. 
      However, PGE2 is known to rapidly undergo nonenzymatic dehydration to produce 
      PGA2, a member of the cyclopentenone PGs, which have been implicated in 
      anti-inflammatory processes. METHODS: In a side-by-side analysis we therefore 
      compared the influence of PGE2 and PGA2 on the TNF-alpha-induced maturation of 
      human moDCs. Phenotypic changes, migratory responses towards MIP-3beta, and 
      T-cell responses induced by the differentially matured moDCs were assessed. 
      RESULTS: We found that PGA2 is nearly as potent as PGE2 in costimulating the 
      TNF-alpha-induced phenotypic maturation of human moDCs. Both PGE2 and PGA2 
      further enhanced the migratory and T-cell-stimulatory capacity of 
      TNF-alpha-treated moDCs. Maturation of moDCs with either PGE2 or PGA2 resulted in 
      enhanced IFN-gamma, TNF-alpha, and IL-5 production and repressed IL-10 production 
      in allogeneic mixed leukocyte cultures. PGE2 was always more potent than PGA2. 
      CONCLUSIONS: Our data suggest that some of the effects attributed to PGE2 may in 
      fact be mediated by its degradation product PGA2. This work also demonstrates 
      that cyclopentenone PGs may have pro-inflammatory properties and that both PGE2 
      and PGA2 can contribute to the development of Th1-type immune responses.
FAU - Thurnher, Martin
AU  - Thurnher M
AD  - Department of Urology & kompetenzzentrum medizin tirol (kmt), Medical University 
      of Innsbruck, Innsbruck, Austria. martin.thurnher@uibk.ac.at
FAU - Putz, Thomas
AU  - Putz T
FAU - Gander, Hubert
AU  - Gander H
FAU - Rahm, Andrea
AU  - Rahm A
FAU - Bartsch, Georg
AU  - Bartsch G
FAU - Ramoner, Reinhold
AU  - Ramoner R
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Exp Hematol
JT  - Experimental hematology
JID - 0402313
RN  - 0 (Adjuvants, Immunologic)
RN  - 0 (Prostaglandins A)
RN  - K6VT5BDY9E (prostaglandin A2)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Adjuvants, Immunologic/pharmacology
MH  - Cells, Cultured
MH  - Chemotaxis, Leukocyte
MH  - Dendritic Cells/*cytology/drug effects/immunology
MH  - Dinoprostone/pharmacology
MH  - Flow Cytometry
MH  - Humans
MH  - Monocytes/*cytology/physiology
MH  - Prostaglandins A/*pharmacology
EDAT- 2005/01/29 09:00
MHDA- 2005/04/12 09:00
CRDT- 2005/01/29 09:00
PHST- 2004/11/01 00:00 [received]
PHST- 2004/11/16 00:00 [accepted]
PHST- 2005/01/29 09:00 [pubmed]
PHST- 2005/04/12 09:00 [medline]
PHST- 2005/01/29 09:00 [entrez]
AID - S0301-472X(04)00414-X [pii]
AID - 10.1016/j.exphem.2004.11.012 [doi]
PST - ppublish
SO  - Exp Hematol. 2005 Feb;33(2):144-50. doi: 10.1016/j.exphem.2004.11.012.