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CRTH2 mediates the activation of human Th2 cells in response to PGD2 released from IgE/anti-IgE treated nasal polyp tissue

Claudina Perez Novo UGent, Gabriële Holtappels UGent, Shân L Vinall, Luzheng Xue, Nan Zhang UGent, Claus Bachert UGent and Roy Pettipher (2010) ALLERGY. 65(3). p.304-310
abstract
BACKGROUND: Mast cells release mediators upon stimulation that contribute to the pathogenesis of chronic airway disease, including the recruitment and activation of Th2 lymphocytes. The objective was to determine the involvement of prostaglandin D(2) (PGD(2)) and its receptors in the chemotaxis of Th2 cells, using nasal polyp tissue. METHODS: Tissue explants from ten patients with nasal polyposis were incubated with RPMI alone or RPMI containing IgE/anti-IgE for 30 min. Some samples were treated with diclofenac to inhibit the production of PGD(2). Supernatants were assayed for PGD(2) content and for their ability to promote human Th2 cell chemotaxis in the presence and absence of a CRTH2 antagonist. Transcript levels of D protanoid receptor type 1 (DP(1)), chemoattractant receptor-homologous receptor expressed on Th2 cells (CRTH2) and PGD(2) synthase were analysed by real time PCR. RESULTS: Increased release of PGD(2) by nasal polyp tissue treated with IgE/anti-IgE was significantly inhibited by preincubation of the tissue with diclofenac. Transcript levels of PGD(2) synthase, DP(1) and CRTH2 receptors increased after stimulation with IgE/anti-IgE. Supernatants from IgE/anti-IgE-stimulated nasal polyp tissue caused significantly increased chemotaxis of Th2 cells. The levels of PGD(2) produced and the degree of Th2 cell chemotaxis were highly correlated. Diclofenac inhibited the production of Th2 cell chemotactic activity, and the chemotactic effect of the supernatant on Th2 cells was inhibited by the CRTH2 antagonist ramatroban. CONCLUSION: These data suggest that in immunologically activated nasal polyp tissue, PGD(2) produced by mast cells promotes the migration of Th2 cells through a CRTH2 dependent mechanism.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
CRTH2, Prostaglandin D2, anti-IgE, chemotaxis, upper airways, Th2 cells
journal title
ALLERGY
Allergy
volume
65
issue
3
pages
304 - 310
Web of Science type
Article
Web of Science id
000274260700005
JCR category
ALLERGY
JCR impact factor
6.297 (2010)
JCR rank
2/20 (2010)
JCR quartile
1 (2010)
ISSN
0105-4538
DOI
10.1111/j.1398-9995.2009.02204.x
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
954487
handle
http://hdl.handle.net/1854/LU-954487
date created
2010-05-27 09:34:20
date last changed
2012-01-23 12:20:54
@article{954487,
  abstract     = {BACKGROUND: Mast cells release mediators upon stimulation that contribute to the pathogenesis of chronic airway disease, including the recruitment and activation of Th2 lymphocytes. The objective was to determine the involvement of prostaglandin D(2) (PGD(2)) and its receptors in the chemotaxis of Th2 cells, using nasal polyp tissue. METHODS: Tissue explants from ten patients with nasal polyposis were incubated with RPMI alone or RPMI containing IgE/anti-IgE for 30 min. Some samples were treated with diclofenac to inhibit the production of PGD(2). Supernatants were assayed for PGD(2) content and for their ability to promote human Th2 cell chemotaxis in the presence and absence of a CRTH2 antagonist. Transcript levels of D protanoid receptor type 1 (DP(1)), chemoattractant receptor-homologous receptor expressed on Th2 cells (CRTH2) and PGD(2) synthase were analysed by real time PCR. RESULTS: Increased release of PGD(2) by nasal polyp tissue treated with IgE/anti-IgE was significantly inhibited by preincubation of the tissue with diclofenac. Transcript levels of PGD(2) synthase, DP(1) and CRTH2 receptors increased after stimulation with IgE/anti-IgE. Supernatants from IgE/anti-IgE-stimulated nasal polyp tissue caused significantly increased chemotaxis of Th2 cells. The levels of PGD(2) produced and the degree of Th2 cell chemotaxis were highly correlated. Diclofenac inhibited the production of Th2 cell chemotactic activity, and the chemotactic effect of the supernatant on Th2 cells was inhibited by the CRTH2 antagonist ramatroban. CONCLUSION: These data suggest that in immunologically activated nasal polyp tissue, PGD(2) produced by mast cells promotes the migration of Th2 cells through a CRTH2 dependent mechanism.},
  author       = {Perez Novo, Claudina and Holtappels, Gabri{\"e}le and Vinall , Sh{\^a}n L and Xue, Luzheng  and Zhang, Nan and Bachert, Claus and Pettipher, Roy},
  issn         = {0105-4538},
  journal      = {ALLERGY},
  keyword      = {CRTH2,Prostaglandin D2,anti-IgE,chemotaxis,upper airways,Th2 cells},
  language     = {eng},
  number       = {3},
  pages        = {304--310},
  title        = {CRTH2 mediates the activation of human Th2 cells in response to PGD2 released from IgE/anti-IgE treated nasal polyp tissue},
  url          = {http://dx.doi.org/10.1111/j.1398-9995.2009.02204.x},
  volume       = {65},
  year         = {2010},
}

Chicago
Perez Novo, Claudina, Gabriële Holtappels, Shân L Vinall , Luzheng Xue, Nan Zhang, Claus Bachert, and Roy Pettipher. 2010. “CRTH2 Mediates the Activation of Human Th2 Cells in Response to PGD2 Released from IgE/anti-IgE Treated Nasal Polyp Tissue.” Allergy 65 (3): 304–310.
APA
Perez Novo, C., Holtappels, G., Vinall , S. L., Xue, L., Zhang, N., Bachert, C., & Pettipher, R. (2010). CRTH2 mediates the activation of human Th2 cells in response to PGD2 released from IgE/anti-IgE treated nasal polyp tissue. ALLERGY, 65(3), 304–310.
Vancouver
1.
Perez Novo C, Holtappels G, Vinall SL, Xue L, Zhang N, Bachert C, et al. CRTH2 mediates the activation of human Th2 cells in response to PGD2 released from IgE/anti-IgE treated nasal polyp tissue. ALLERGY. 2010;65(3):304–10.
MLA
Perez Novo, Claudina, Gabriële Holtappels, Shân L Vinall , et al. “CRTH2 Mediates the Activation of Human Th2 Cells in Response to PGD2 Released from IgE/anti-IgE Treated Nasal Polyp Tissue.” ALLERGY 65.3 (2010): 304–310. Print.