Increased Expression of Thymic Stromal Lymphopoietin and Its Receptor in Kimura's Disease

• Published in: O.R.L. Journal for oto-rhino-laryngology and its related specialties Vol. 77; no. 1; pp. 44 - 54
• Main Authors: Sakitani, Eri, Nonaka, Manabu, Shibata, Noriyuki, Furukawa, Toru, Yoshihara, Toshio
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland S. Karger AG 01.01.2015
• Subjects: Adolescent; Adult; Aged; Angiolymphoid Hyperplasia with Eosinophilia - etiology; Angiolymphoid Hyperplasia with Eosinophilia - metabolism; Angiolymphoid Hyperplasia with Eosinophilia - pathology; Case-Control Studies; Cytokines - genetics; Cytokines - metabolism; Drug therapy; Female; Gene expression; Humans; Interleukin-17 - genetics; Interleukin-17 - metabolism; Interleukin-33 - genetics; Interleukin-33 - metabolism; Male; Middle Aged; Neurons; Original Paper; Parotid Gland - metabolism; Receptors, Cytokine - genetics; Receptors, Cytokine - metabolism; Ribonucleic acid; RNA; RNA, Messenger - metabolism; Young Adult; Massively parallel sequencing; Thymic stromal lymphopoietin; Serial analysis of gene expression; Kimuraߣs disease; Mast cells; Thymic stromal lymphopoietin receptor; Macrophages
• ISSN: 0301-1569; 1423-0275; 1423-0275
• DOI: 10.1159/000371424

Objective: The objective of this study was to investigate the expression of thymic stromal lymphopoietin (TSLP) and TSLP receptor (TSLPR) in Kimura's disease (KD). Methods: Using parotid gland tissues from KD patients and control subjects, we quantified the expression levels of mRNA for TSLP, interleukin (IL)-25, IL-33, and their receptors by massively parallel sequencing. We also performed immunohistochemical analysis of TSLP and TSLPR, and counted cells immunoreactive for these proteins by the polymer immunocomplex and double immunofluorescence methods. Results: The levels of mRNA for TSLP, TSLPR, and IL-25R, but not IL-25, IL-33, or IL-33R, were significantly elevated in parotid gland tissues from the KD group as compared to the control group. Immunohistochemical analysis revealed that TSLP- and TSLPR-positive cells were significantly increased in number in parotid gland tissues from KD patients. Double immunofluorescence staining showed that TSLP and TSLPR were localized mainly in CD68-positive macrophages and tryptase-positive mast cells, respectively. Conclusions: Overexpression of TSLP and TSLPR might contribute to the pathogenesis of KD through interactions between macrophages and mast cells. Regulation of TSLP/TSLPR signaling may be a potential therapeutic approach for KD.