Δ12-Prostaglandin D2 is a potent and selective CRTH2 receptor agonist and causes activation of human eosinophils and Th2 lymphocytes

Gazi, Lucien; Gyles, Shân L.; Rose, Jennifer; Lees, Sally; Allan, Chris; Xue, Luzheng; Jassal, Ramesh; Speight, Graham; Gamble, Vicki; Pettipher, Roy

doi:10.1016/j.prostaglandins.2004.11.003

Cited by 42 publications

(42 citation statements)

References 32 publications

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“…This hypothetical mechanism was confirmed by a significant increase in WBC count and lymphocyte percent in contrast to other WBC cells (Table 2). This allergic reaction could be mediated by proinflammatory effects of prostaglandin D2 released by WBC cells like lymphocytes with inhibitory effects on hair growth in AGA patients [42].…”

Section: Discussionmentioning

confidence: 99%

Androgenetic Alopecia: A Chronic or Pubertal Onset Disease Retarded by Blood Donation

Dayer

Dehghani

Daer³

et al. 2017

Zahedan J Res Med Sci

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Background: Androgenetic alopecia is the main cause of hair loss and common baldness that affects psychological more than physiological aspects of people's lives. Studies have shown that this multi factorial disorder is initiated by androgens secretion in pubertal period, minerals limitations, autoimmunity, mental stress, genetic predisposition and some alterations in hematological factors. Objectives: The aim of this study was to evaluate the involvement of hematologic parameters in this disease using a case control study design. Methods: In this case-controlled study, two groups each of 80 individuals with androgenetic alopecia were voluntarily included in the study based on their medical histories and clinical examinations and subjected to blood tests for routine hematological parameters. The results were then compared and analyzed using SPSS version 16.0.

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Section: Discussionmentioning

confidence: 99%

Androgenetic Alopecia: A Chronic or Pubertal Onset Disease Retarded by Blood Donation

Dayer

Dehghani

Daer³

et al. 2017

Zahedan J Res Med Sci

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“…Calcium mobilization in human Th2 cells was stimulated by CRTH2 agonists (PGD 2 and DK-PGD 2 ) but not by the DP selective agonist (BW245C) (22). PGD 2 and BW245C both demonstrated low efficacy on cAMP signaling in Th2 cells (Fig.…”

Section: Crth2 Is the Dominant Receptor Mediating Pgd 2 Signals In Humentioning

confidence: 91%

“…Th2 cells were prepared using a modified method described previously (22). Briefly, PBMC were isolated from buffy coats (National Blood Service) by Ficoll-Hypaque (Amersham Biosciences) density gradient centrifugation, followed by CD4-positive cell purification using MACS CD4 ϩ T FIGURE 1.…”

Section: Culture Of Th2 Cellsmentioning

confidence: 99%

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Prostaglandin D2 Causes Preferential Induction of Proinflammatory Th2 Cytokine Production through an Action on Chemoattractant Receptor-Like Molecule Expressed on Th2 Cells

Xue

Gyles

Wettey

et al. 2005

The Journal of Immunology

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238

205

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PGD2, produced by mast cells, has been detected in high concentrations at sites of allergic inflammation. It can stimulate vascular and other inflammatory responses by interaction with D prostanoid receptor (DP) and chemoattractant receptor-like molecule expressed on Th2 cells (CRTH2) receptors. A significant role for PGD2 in mediating allergic responses has been suggested based on the observation that enhanced eosinophilic lung inflammation and cytokine production is apparent in the allergen-challenged airways of transgenic mice overexpressing human PGD2 synthase, and PGD2 can enhance Th2 cytokine production in vitro from CD3/CD28-costimulated Th2 cells. In the present study, we investigated whether PGD2 has the ability to stimulate Th2 cytokine production in the absence of costimulation. At concentrations found at sites of allergic inflammation, PGD2 preferentially elicited the production of IL-4, IL-5, and IL-13 by human Th2 cells in a dose-dependent manner without affecting the level of the anti-inflammatory cytokine IL-10. Gene transcription peaked within 2 h, and protein release peaked ∼8 h after stimulation. The effect of PGD2 was mimicked by the selective CRTH2 agonist 13,14-dihydro-15-keto-PGD2 but not by the selective DP agonist BW245C, suggesting that the stimulation is mediated by CRTH2 and not DP. Ramatroban, a dual CRTH2/thromboxane-like prostanoid receptor antagonist, markedly inhibited Th2 cytokine production induced by PGD2, while the selective thromboxane-like prostanoid receptor antagonist SQ29548 was without effect. These data suggest that PGD2 preferentially up-regulates proinflammatory cytokine production in human Th2 cells through a CRTH2-dependent mechanism in the absence of any other costimulation and highlight the potential utility of CRTH2 antagonists in the treatment of allergic diseases.

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“…In this regard, it is noteworthy that prostaglandin D 2 and reactive oxygen species both initiate and/or augment Th2-related inflammation. 155,156 Cytokines Regulate Protease Activities Associated With AAA Development Cytokines regulate MMP, serine protease, and cathepsin expression. Indeed, both Th1 and Th2 cytokines (eg, IFN-␥ or IL-4) induce or inhibit the expression of specific MMP, depending on the particular experimental conditions.…”

Section: Patterns Of Cytokine Expression In Stenotic Versus Aneurysmamentioning

confidence: 99%

Vascular Remodeling in Transplant Vasculopathy

Mitchell

Libby

2007

Circulation Research

238

216

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Abstract-As therapeutic strategies to prevent acute rejection progressively improve, transplant vasculopathy (TV)constitutes the single most important limitation for long-term functioning of solid organ allografts. In TV, allograft arteries characteristically develop severe, diffuse intimal hyperplastic lesions that eventually compromise luminal flow and cause ischemic graft failure. Traditional immunosuppressive strategies that check acute allograft rejection do not prevent TV; indeed 50% of transplant recipients will have significant disease within five years of organ transplantation, and 90% will have significant TV a decade after their surgery. TV can involve the entire length of the transplanted arterial bed, including penetrating intraorgan arterioles. Indeed, the luminal narrowing of such penetrating vessels may be the most functionally significant because arterioles represent the major contributors to tissue vascular resistance. Because of the diffuseness of TV involvement in the allograft vascular bed, the only currently definitive therapy requires re-transplantation. Nevertheless, as we better understand the pathogenesis and critical mediators of these lesions, pharmacological advances can be anticipated. Other articles in this thematic review series focus on the specifics of the inciting injury, the cytokines and chemokines that drive TV development, and the nature of the recruited cells in TV lesions, as well as the pathogenic similarities between TV and other vascular lesions such as atherosclerosis. This review focuses on the mechanisms of vascular wall remodeling in TV, including the intimal accumulation of smooth muscle-like cells and associated extracellular matrix, medial smooth muscle cell degeneration, and adventitial fibrosis. A brief overview highlights the aneurysmal changes that can accrue when vessel wall inflammation has a cytokine profile distinct from the typical proinflammatory interferon-␥-dominated milieu. We and others showed that the development of TV requires the archetypal Th1 cytokine interferon-␥ (IFN-␥); TV lesions do not develop in the setting of congenital absence or monoclonal antibody blockade of IFN-␥. 8,11,12 In an elegant experiment using donor human arterial grafts in immunodeficient mice, Tellides et al further demonstrated that IFN-␥ alone, without associated inflammation, is sufficient to induce TV-like lesions. 13 However, despite almost a decade of subsequent investigation, the relevant IFN-␥ pathway(s) underlying TV development remain ill defined. As discussed elsewhere in this review series (G. Tellides and J. Pober), the potent pleiotropic cytokine IFN-␥ affects the activation state of multiple cell types, and also regulates major histocompatibility complex and costimulator molecule expression and the production of cytokines, chemokines, adhesion molecules, and extracellular matrix (ECM). Classically a product of Th1 and Tc1 T-cell subsets as well as natural killer (NK) cells, IFN-␥ also can be produced by activated macrophages (forming an autocrine loop), 14...

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Δ12-Prostaglandin D2 is a potent and selective CRTH2 receptor agonist and causes activation of human eosinophils and Th2 lymphocytes

Cited by 42 publications

References 32 publications

Androgenetic Alopecia: A Chronic or Pubertal Onset Disease Retarded by Blood Donation

Androgenetic Alopecia: A Chronic or Pubertal Onset Disease Retarded by Blood Donation

Prostaglandin D2 Causes Preferential Induction of Proinflammatory Th2 Cytokine Production through an Action on Chemoattractant Receptor-Like Molecule Expressed on Th2 Cells

Vascular Remodeling in Transplant Vasculopathy

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