Jae Ho Lee1, Seung-Ki Kwok2, Seung Min Jung1, Jennifer Lee1, Jae-Seon Lee1, Seung Ye Baek1, Eun-Kyung Kim1, Ji Hyeon Ju1, Sung-Hwan Park1, Ho-Youn Kim1. 1. From the Division of Rheumatology, Department of Internal Medicine, School of Medicine, and the Rheumatism Research Center, The Catholic University of Korea, Seoul, South Korea.J.H. Lee, MD, Bachelor's degree, Appointment Physician, Rheumatology Specialist, Fellow; S-K. Kwok, MD, PhD, Appointment Physician, Rheumatology Specialist, Associate Professor; S.M. Jung, MD, Bachelor's degree, Appointment Physician, Rheumatology Specialist, Fellow; J. Lee, MD, Bachelor's degree, Appointment Physician, Rheumatology Specialist, Fellow; J.H. Ju, MD, PhD, Appointment Physician, Rheumatology Specialist, Associate Professor; S-H. Park, MD, PhD, Appointment Physician, Rheumatology Specialist, Professor; H-Y. Kim, MD, PhD, Appointment Physician, Rheumatology Specialist, Professor, Division of Rheumatology, Department of Internal Medicine, School of Medicine; J-S. Lee, Master's degree, Appointment Researcher; S.Y. Baek, Bachelor's degree, Appointment Researcher; E-K. Kim, Bachelor's degree, Appointment Researcher, Rheumatism Research Center, The Catholic University of Korea. 2. From the Division of Rheumatology, Department of Internal Medicine, School of Medicine, and the Rheumatism Research Center, The Catholic University of Korea, Seoul, South Korea.J.H. Lee, MD, Bachelor's degree, Appointment Physician, Rheumatology Specialist, Fellow; S-K. Kwok, MD, PhD, Appointment Physician, Rheumatology Specialist, Associate Professor; S.M. Jung, MD, Bachelor's degree, Appointment Physician, Rheumatology Specialist, Fellow; J. Lee, MD, Bachelor's degree, Appointment Physician, Rheumatology Specialist, Fellow; J.H. Ju, MD, PhD, Appointment Physician, Rheumatology Specialist, Associate Professor; S-H. Park, MD, PhD, Appointment Physician, Rheumatology Specialist, Professor; H-Y. Kim, MD, PhD, Appointment Physician, Rheumatology Specialist, Professor, Division of Rheumatology, Department of Internal Medicine, School of Medicine; J-S. Lee, Master's degree, Appointment Researcher; S.Y. Baek, Bachelor's degree, Appointment Researcher; E-K. Kim, Bachelor's degree, Appointment Researcher, Rheumatism Research Center, The Catholic University of Korea. seungki73@catholic.ac.kr.
Abstract
OBJECTIVE: To investigate the expression of fractalkine and identify the clinical effects of fractalkine and its receptor (CX3CR1) in patients with primary Sjögren syndrome (pSS). METHODS: Serum fractalkine levels were determined by ELISA. Immunohistochemical staining was done to compare the expression of fractalkine and CX3CR1 between salivary glands (SG) of patients with SS and controls. The cells to be merged with fractalkine were evaluated by confocal microscopy. Type of CX3CR1-expressing cells among infiltrating lymphocytes in SG was analyzed by confocal microscopy. Further, associations among fractalkine, proinflammatory cytokines, and clinical profiles were investigated. RESULTS: Serum fractalkine levels in patients with pSS were higher than those in the control group (p = 0.026). SG expression of fractalkine and its receptor was upregulated in patients with pSS compared to that in the controls by immunohistochemistry. Higher histological grade was associated with more fractalkine-positive cells per total epithelial cells. Epithelial cells were the main fractalkine-expressing cell type in the SG. Serum fractalkine levels were significantly correlated with proinflammatory cytokines levels (interleukin 17: r = 0.685, p = 0.029; tumor necrosis factor-α: r = 0.444, p = 0.003), antinuclear antibody (r = 0.349, p = 0.022), and immunoglobulin G levels (r = 0.325, p = 0.044). Serum fractalkine levels in patients with extraglandular manifestations of pSS were significantly higher than in those without extraglandular manifestations (p = 0.026). CONCLUSION: Fractalkine and CX3CR1 may play a role in the pathogenesis of pSS, including extraglandular manifestations.
OBJECTIVE: To investigate the expression of fractalkine and identify the clinical effects of fractalkine and its receptor (CX3CR1) in patients with primary Sjögren syndrome (pSS). METHODS: Serum fractalkine levels were determined by ELISA. Immunohistochemical staining was done to compare the expression of fractalkine and CX3CR1 between salivary glands (SG) of patients with SS and controls. The cells to be merged with fractalkine were evaluated by confocal microscopy. Type of CX3CR1-expressing cells among infiltrating lymphocytes in SG was analyzed by confocal microscopy. Further, associations among fractalkine, proinflammatory cytokines, and clinical profiles were investigated. RESULTS: Serum fractalkine levels in patients with pSS were higher than those in the control group (p = 0.026). SG expression of fractalkine and its receptor was upregulated in patients with pSS compared to that in the controls by immunohistochemistry. Higher histological grade was associated with more fractalkine-positive cells per total epithelial cells. Epithelial cells were the main fractalkine-expressing cell type in the SG. Serum fractalkine levels were significantly correlated with proinflammatory cytokines levels (interleukin 17: r = 0.685, p = 0.029; tumor necrosis factor-α: r = 0.444, p = 0.003), antinuclear antibody (r = 0.349, p = 0.022), and immunoglobulin G levels (r = 0.325, p = 0.044). Serum fractalkine levels in patients with extraglandular manifestations of pSS were significantly higher than in those without extraglandular manifestations (p = 0.026). CONCLUSION:Fractalkine and CX3CR1 may play a role in the pathogenesis of pSS, including extraglandular manifestations.
Authors: A de St Maurice; E Ervin; R Orone; M Choi; E K Dokubo; P E Rollin; S T Nichol; D Williams; J Brown; R Sacra; J Fankhauser; B Knust Journal: Open Forum Infect Dis Date: 2018-09-21 Impact factor: 3.835