alexa CRTH2 is Critical to the Development of Colitis Induced by Dextran Sodium Sulfate (DSS)
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Research Article

CRTH2 is Critical to the Development of Colitis Induced by Dextran Sodium Sulfate (DSS)

Hak-Ling Ma1, Debra Goodwin1, Susan Fish1, Lee Napierata1, Paul Morgan2, Karen Page2, Aaron R Winkler2, Katherine Masek-Hammerman3, Zaher Radi3, Eddine Saiah4, Neelu Kaila4 and Cara M. M. Williams2*
1Immunology and Autoimmunity, Pfizer WR&D, Cambridge, MA, USA
2Inflammation and Remodeling, Pfizer WR&D, Cambridge, MA, USA
3Drug Safety Research &Development, Pfizer WR&D, Cambridge, MA, USA
4Medicinal Chemistry, Pfizer WR&D, Cambridge, MA, USA
Corresponding Author : Cara M. M. Williams, PhD
Inflammation and Remodeling Research Unit
Pfizer Worldwide research and Development
200 Cambridge Park Drive, Cambridge, MA 02140, USA
Tel: 617-665-5920
Fax: 617-665-5584
E-mail: [email protected]
Received February 20, 2012; Accepted June 20, 2012; Published June 29, 2012
Citation: Ma HL, Goodwin D, Fish S, Napierata L, Morgan P, et al. (2012) CRTH2 is Critical to the Development of Colitis Induced by Dextran Sodium Sulfate (DSS). J Clin Cell Immunol 3:131. doi:10.4172/2155-9899.1000131
Copyright: © 2012 Ma HL, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Chemoattractant Receptor-homologous molecule expressed on Th2 cells [CRTH2] is expressed on granulocytes (eosinophils, basophils and neutrophils), Th2 cells and monocytes. CRTH2 has been implicated in the development of cutaneous inflammation as CRTH2+ CD4+ T cells and CRTH2+ eosinophils are increased in the blood of atopic dermatitis patients. CRTH2 is also up-regulated in circulating neutrophils of psoriatic patients. Interestingly, CRTH2 is detected in the mucosa of patients with Inflammatory Bowel Disease (IBD) ulcerative colitis, where the CRTH2 positive cells localize within and adjacent to regions of inflamed mucosa suggesting that CRTH2 may play a role in IBD. However, the exact downstream inflammatory pathways resulting from CRTH2 activation in colitis are not well characterized. To gain a better understanding of the effects of CRTH2 activation in the pathogenesis of colitis, we have generated a small molecule inhibitor against CRTH2 and its potency was first validated in an oxazolone induced contact dermatitis model. We investigated the consequences of inhibiting CRTH2 in the development of IBD using a Dextran Sodium Sulfate (DSS)-induced colitis mouse model. Compared to the vehicle control group, mice treated with a selective CRTH2 antagonist had reduced disease severity as measured by weight loss, as well as serum acute phase protein, haptoglobin. Furthermore, pro-inflammatory cytokine gene expression for TNFα, IL-1β, IL-6, IL-17A, and IFNγ were reduced in colons of mice that had been treated with the CRTH2 antagonist compared with DSS treated controls that received vehicle. Taken together, our data identify a previously unrecognized role for CRTH2 in the initiation/amplification and/or stabilization of colon inflammation.

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