Esophageal human β-defensin expression in eosinophilic esophagitis

Shauna Schroeder, Zachary D. Robinson, Joanne C. Masterson, Lindsay Hosford, Wendy Moore, Zhaoxing Pan, Rachel Harris, Rhonda F. Souza, Stuart Jon Spechler, Sophie A. Fillon, Glenn T. Furuta

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background: Defensins are antimicrobial peptides expressed on mucosal surfaces that contribute to maintaining intestinal homeostasis by providing innate defense mechanisms for the epithelia. Defensin expression is altered in a number of diseases that affect mucosal surfaces, such as atopic dermatitis, allergic rhinitis, and inflammatory bowel disease. Similar to atopic dermatitis, eosinophilic esophagitis (EoE) is a chronic disease in which the squamous epithelial surface is affected by a similar T H 2 microenvironment and eosinophil-predominant inflammation. Therefore, we hypothesized that defensin expression would be decreased in EoE. Methods: To address this, we measured defensin expression in vitro in cell lines derived from patients with EoE (EoE1-T) or gastroesophageal reflux disease (GERD) (NES-G4T cells) and ex vivo in esophageal mucosal biopsy samples from children with EoE or GERD and control children without esophageal disease. Results: Interleukin-5 induced a decrease in human β-defensin (hBD)-1 and hBD3 expression in EoE1-T but not in NES-G4T cells. Compared with esophageal biopsy specimens from GERD and control children, specimens from EoE pediatric patients revealed a significant decrease in mRNA and protein expression for hBD1 and hBD3. Conclusion: Diminished expression of hBD1 and hBD3 may make the esophageal epithelium more susceptible to the development and/or perpetuation of EoE.

Original languageEnglish (US)
Pages (from-to)647-654
Number of pages8
JournalPediatric Research
Volume73
Issue number5
DOIs
StatePublished - May 2013

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Eosinophilic Esophagitis
Defensins
Gastroesophageal Reflux
Atopic Dermatitis
Epithelium
Esophageal Diseases
Biopsy
Interleukin-5
Inflammatory Bowel Diseases
Eosinophils
Homeostasis
Chronic Disease
Pediatrics
Inflammation
Cell Line
Messenger RNA
Peptides

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Cite this

Schroeder, S., Robinson, Z. D., Masterson, J. C., Hosford, L., Moore, W., Pan, Z., ... Furuta, G. T. (2013). Esophageal human β-defensin expression in eosinophilic esophagitis. Pediatric Research, 73(5), 647-654. https://doi.org/10.1038/pr.2013.23

Esophageal human β-defensin expression in eosinophilic esophagitis. / Schroeder, Shauna; Robinson, Zachary D.; Masterson, Joanne C.; Hosford, Lindsay; Moore, Wendy; Pan, Zhaoxing; Harris, Rachel; Souza, Rhonda F.; Jon Spechler, Stuart; Fillon, Sophie A.; Furuta, Glenn T.

In: Pediatric Research, Vol. 73, No. 5, 05.2013, p. 647-654.

Research output: Contribution to journalArticle

Schroeder, S, Robinson, ZD, Masterson, JC, Hosford, L, Moore, W, Pan, Z, Harris, R, Souza, RF, Jon Spechler, S, Fillon, SA & Furuta, GT 2013, 'Esophageal human β-defensin expression in eosinophilic esophagitis', Pediatric Research, vol. 73, no. 5, pp. 647-654. https://doi.org/10.1038/pr.2013.23
Schroeder S, Robinson ZD, Masterson JC, Hosford L, Moore W, Pan Z et al. Esophageal human β-defensin expression in eosinophilic esophagitis. Pediatric Research. 2013 May;73(5):647-654. https://doi.org/10.1038/pr.2013.23
Schroeder, Shauna ; Robinson, Zachary D. ; Masterson, Joanne C. ; Hosford, Lindsay ; Moore, Wendy ; Pan, Zhaoxing ; Harris, Rachel ; Souza, Rhonda F. ; Jon Spechler, Stuart ; Fillon, Sophie A. ; Furuta, Glenn T. / Esophageal human β-defensin expression in eosinophilic esophagitis. In: Pediatric Research. 2013 ; Vol. 73, No. 5. pp. 647-654.
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AU - Moore, Wendy

AU - Pan, Zhaoxing

AU - Harris, Rachel

AU - Souza, Rhonda F.

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AB - Background: Defensins are antimicrobial peptides expressed on mucosal surfaces that contribute to maintaining intestinal homeostasis by providing innate defense mechanisms for the epithelia. Defensin expression is altered in a number of diseases that affect mucosal surfaces, such as atopic dermatitis, allergic rhinitis, and inflammatory bowel disease. Similar to atopic dermatitis, eosinophilic esophagitis (EoE) is a chronic disease in which the squamous epithelial surface is affected by a similar T H 2 microenvironment and eosinophil-predominant inflammation. Therefore, we hypothesized that defensin expression would be decreased in EoE. Methods: To address this, we measured defensin expression in vitro in cell lines derived from patients with EoE (EoE1-T) or gastroesophageal reflux disease (GERD) (NES-G4T cells) and ex vivo in esophageal mucosal biopsy samples from children with EoE or GERD and control children without esophageal disease. Results: Interleukin-5 induced a decrease in human β-defensin (hBD)-1 and hBD3 expression in EoE1-T but not in NES-G4T cells. Compared with esophageal biopsy specimens from GERD and control children, specimens from EoE pediatric patients revealed a significant decrease in mRNA and protein expression for hBD1 and hBD3. Conclusion: Diminished expression of hBD1 and hBD3 may make the esophageal epithelium more susceptible to the development and/or perpetuation of EoE.

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