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• W2029679947 abstract "atopic dermatitis gastrin-releasing peptide GRP receptor protein gene product visual analog scale TO THE EDITOR Bombesin and two major bombesin-like peptides in mammals, gastrin-releasing peptide (GRP) and neuromedin B, have been shown to elicit various physiological effects. GRP elicits gastrin release and regulates gastric acid secretion and motor function (Merali et al., 1999Merali Z. McIntosh J. Anisman H. Role of bombesin-related peptides in the control of food intake.Neuropeptides. 1999; 33: 376-386Abstract Full Text PDF PubMed Scopus (95) Google Scholar. This peptide is also involved in the biology of the circadian system. Interestingly, intradermal injections of GRP elicit scratching in mice (Andoh et al., 2011Andoh T. Kuwazono T. Lee J.B. et al.Gastrin-releasing peptide induces itch-related responses through mast cell degranulation in mice.Peptides. 2011; 32: 2098-2103Crossref PubMed Scopus (36) Google Scholar. GRP is expressed in a subset of peptidergic dorsal root ganglion neurons, whereas GRP receptor (GRPR) is expressed in lamina I of the dorsal spinal cord (Sun and Chen, 2007Sun Y.G. Chen Z.F. A gastrin-releasing peptide receptor mediates the itch sensation in the spinal cord.Nature. 2007; 448: 700-703Crossref PubMed Scopus (571) Google Scholar. When lamina I neurons expressing GRPR in the spinal cord were selectively ablated, the mice showed profound scratching deficits in response to all of the itching stimuli tested, irrespective of their histamine dependence (Sun et al., 2009Sun Y.G. Zhao Z.Q. Meng X.L. et al.Cellular basis of itch sensation.Science. 2009; 325: 1531-1534Crossref PubMed Scopus (449) Google Scholar. These data support the labeled line for itching in the spinal cord and provide an important cellular basis for explaining how a pruritogenic stimulus is perceived by the brain as a major sensation. Atopic dermatitis (AD) is an inflammatory pruritic skin disorder. Mechanical trauma resulting from extensive scratching that is precipitated by intensive itching results in skin barrier dysfunction and exacerbation of AD (Barnes, 2010Barnes K.C. An update on the genetics of atopic dermatitis: scratching the surface in 2009.J Allergy Clin Immunol. 2010; 125: 16-29Abstract Full Text Full Text PDF PubMed Scopus (247) Google Scholar. So far, severe pruritus in AD has been attributed to increased release of substance P, nerve growth factor, neurotrophin-3 and 4, brain-derived neurotrophic factor, histamine, and IL-31 (Arck and Paus, 2006Arck P. Paus R. From the brain-skin connection: the neuroendocrine-immune misalliance of stress and itch.Neuroimmunomodulation. 2006; 13: 347-356Crossref PubMed Scopus (104) Google Scholar; Lee et al., 2006Lee C.H. Chuang H.Y. Shih C.C. et al.Transepidermal water loss, serum IgE and beta-endorphin as important and independent biological markers for development of itch intensity in atopic dermatitis.Br J Dermatol. 2006; 154: 1100-1107Crossref PubMed Scopus (101) Google Scholar; Scuri et al., 2010Scuri M. Samsell L. Piedimonte G. The role of neurotrophins in inflammation and allergy.Inflamm Allergy Drug Targets. 2010; 9: 173-180Crossref PubMed Scopus (72) Google Scholar; Lee and Yu, 2011Lee C.H. Yu H.S. Biomarkers for itch and disease severity in atopic dermatitis.Curr Probl Dermatol. 2011; 41: 136-148Crossref PubMed Scopus (45) Google Scholar. It was recently reported that a proportion of protein gene product (PGP) 9.5+ nerve fibers expressed GRP in both the epidermis and the dermis of NC/Nga mice, the most popular AD model mice (Tominaga et al., 2009Tominaga M. Ogawa H. Takamori K. Histological characterization of cutaneous nerve fibers containing gastrin-releasing peptide in NC/Nga mice: an atopic dermatitis model.J Invest Dermatol. 2009; 129: 2901-2905Abstract Full Text Full Text PDF PubMed Scopus (60) Google Scholar. In this study, we examined serum GRP levels in AD and their correlation with visual analog scale (VAS) itch scores. A total of 53 AD patients (mean±SD age: 36.4±12.6 years, 31 men and 22 women) and 35 healthy controls (41.6±16.0 years, 11 men and 24 women) were enrolled in this study. All AD patients were given diagnoses according to the criteria of Hanifin and Rajka, 1980Hanifin J.M. Rajka G. Diagnostic features of atopic dermatitis.Acta Derm Venereol Suppl (Stockh). 1980; 92: 44-47Google Scholar. We rated itch by VAS 0–10, asking the patients to mark a point on the line corresponding to mean itch during the last 7 days before blood draw. The medical ethical committee of the University of Tokyo approved all described studies, and the study was conducted according to the Declaration of Helsinki Principles. Informed consent was obtained from participants. The 35 healthy controls had no history of allergy or pruritus. Enzyme immunoassay was performed using GRP EIA kit obtained from Phoenix Pharmaceuticals (Burlingame, CA). Biopsy specimens obtained from AD patients (n=5) and healthy controls (n=6) were snap-frozen, cut into 5-μm-thick cryostat sections, and fixed in acetone. These sections were then stained with rabbit anti-human GRP antibody (number H-027-07, Phoenix Pharmaceuticals) and mouse anti-human PGP 9.5 mAb (13C4/I3C4, Abcam plc, Cambridge, UK), followed by corresponding secondary antibodies labeled with Alexa-Fluor 488 or Alexa-Fluor 594 (Molecular Probes, Eugene, OR). The numbers of double-positive fibers per × 100 field were counted independently by two investigators in a blinded manner. The χ2 goodness-of-fit test was used to evaluate normality for all parameters. The F-test was used to evaluate the equality of variance between two groups. Welch’s t test was used for comparison between two groups. Correlation coefficients were determined by using Spearman’s rank correlation test. P<0.05 was considered significant. Serum GRP levels in AD patients were significantly higher than in healthy individuals (3.11±0.98 and 2±0.58ngml−1, respectively; P<0.001, Figure 1a). When serum GRP levels higher than the mean+2SD of the control serum samples were considered to be elevated, the percentage of elevated samples in AD were 45.2%. We compared serum GRP levels with other laboratory data reflecting disease activity of AD, such as serum levels of IgE, sIL–2R, IL-31, CCL17, and numbers of eosinophils in peripheral blood. There was no significant relation between serum GRP levels and these markers (data not shown). By contrast, there was a significant correlation between serum GRP levels and VAS itch scores (r=0.725, P<0.01, Figure 1b). We next performed double immunofluorescence staining for GRP and PGP 9.5. In both AD lesional skin and normal skin, dermal PGP 9.5+ nerve fibers expressed GRP (Figure 2), as was previously reported in NC/Nga mice. Absorption experiments suggested that immunoreactivity in the epidermis was false-positive (data not shown). The number of GRP+ nerve fibers in AD skin (5.0±1.2 per × 100 field) was significantly larger than that of normal skin (2.7±0.8 per × 100 field).Figure 2Double immunofluorescence staining for gastrin-releasing peptide (GRP) and protein gene product (PGP) 9.5. Dermal PGP 9.5+ nerve fibers (red) expressed GRP (green). Increased numbers of double-positive fibers (yellow) in lesional skin of atopic dermatitis compared with normal skin. Representative two cases in each group. Bar = 100μm.View Large Image Figure ViewerDownload (PPT) We clearly demonstrated that serum GRP levels in AD patients were significantly higher than in healthy individuals, and that they correlated with VAS itch scores. Transepidermal water loss and serum levels of β-endorphin and IgE are useful biomarkers for itch intensity in AD patients (Lee et al., 2006Lee C.H. Chuang H.Y. Shih C.C. et al.Transepidermal water loss, serum IgE and beta-endorphin as important and independent biological markers for development of itch intensity in atopic dermatitis.Br J Dermatol. 2006; 154: 1100-1107Crossref PubMed Scopus (101) Google Scholar. IL-31 is also regarded as a key cytokine for the development of AD-induced skin inflammation and pruritus (Bilsborough et al., 2006Bilsborough J. Leung D.Y. Maurer M. et al.IL-31 is associated with cutaneous lymphocyte antigen-positive skin homing T cells in patients with atopic dermatitis.J Allergy Clin Immunol. 2006; 117: 418-425Abstract Full Text Full Text PDF PubMed Scopus (288) Google Scholar. However, serum IgE and IL-31 levels did not correlate with VAS itch scores in this study. Although further studies with a large number of cases are required, serum GRP levels could be a better biomarker of itch in AD patients. No significant correlation between serum GRP levels and serum IgE or IL-31 levels in this study has also suggested multiple pathways for itch sensation. GRP-induced scratching was inhibited by the μ-opioid receptor antagonist naltrexone hydrochloride, the GRPR antagonist RC-3095, the H1 histamine receptor antagonists fexofenadine hydrochloride and chlorpheniramine maleate, and the PAR2 proteinase-activated receptor antagonist FSLLRY-NH2 (Andoh et al., 2011Andoh T. Kuwazono T. Lee J.B. et al.Gastrin-releasing peptide induces itch-related responses through mast cell degranulation in mice.Peptides. 2011; 32: 2098-2103Crossref PubMed Scopus (36) Google Scholar. It has recently been reported that central GRPR and neuromedin B receptor act independently to elicit scratching behavior and that there is an additional, unidentified receptor mechanism underlying bombesin-elicited scratching (Su and Ko, 2011Su P.Y. Ko M.C. The role of central gastrin-releasing peptide and neuromedin B receptors in the modulation of scratching behavior in rats.J Pharmacol Exp Ther. 2011; 337: 822-829Crossref PubMed Scopus (38) Google Scholar. In summary, elevated serum GRP levels and increased numbers of dermal GRP+ nerve fibers suggested that this peptide could be a therapeutic target for itch in AD patients. We thank Yoshiko Ito and Tamami Kaga for technical assistance. This study was supported by grants from the Ministry of Education, Culture, Sports, and Technology (Japan)." @default.
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• W2029679947 title "Serum Gastrin-Releasing Peptide Levels Correlate with Pruritus in Patients with Atopic Dermatitis" @default.
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