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- Title
Dysregulated interleukin 11 in primary Sjögren's syndrome contributes to apoptosis of glandular epithelial cells.
- Authors
Ye, Lei; Shi, Huan; Wu, Shufeng; Yu, Chuangqi; Wang, Baoli; Zheng, Lingyan
- Abstract
The purpose of this study was to explore the potential function of interleukin‐11 (IL‐11) in the pathogenesis of primary Sjögren's syndrome (pSS) patients. Real‐time polymerase chain reaction was performed to examine IL‐11 expression in the labial glands of 30 pSS patients and 30 healthy controls. Immunohistochemistry was conducted to assess the distribution of IL‐ll‐positive cells in labial glands. The human salivary gland (HSG) cell line was used to study the effects of IL‐11 on gland epithelial cells in vitro. Cell viability and cell proliferation were examined by CCK‐8 kit and EdU assay, respectively. The population of apoptotic cells was detected in flow cytometry followed by Annexin V/PI and Hoechst staining. We found that the expression levels of IL‐11 were remarkably decreased in pSS labial glands and were positively correlated with C‐reactive protein levels and negatively correlated with rheumatoid factor levels. Fewer numbers of glandular epithelial cells were observed to be positively stained with IL‐11 antibody in labial glands from pSS patients than those in healthy control patients. After IL‐11 treatment, the viability and proliferation of HSG cells were significantly higher than those in the control group. The total apoptotic and necrotic rates of HSG cells in the group after IL‐11 treatment were significantly lower. In conclusion, the results indicated that IL‐11 promoted viability and proliferation and inhibited apoptotic and necrotic rates of glandular epithelial cells. In pSS, downregulated IL‐11 might contribute to the apoptosis of salivary gland epithelial cells. However, it might be a potential target to alleviate the pathological atrophy of glandular epithelial cells in pSS patients.
- Subjects
EPITHELIAL cells; CELL populations; CELL survival; SALIVARY glands; RHEUMATOID factor; C-reactive protein
- Publication
Cell Biology International, 2020, Vol 44, Issue 1, p327
- ISSN
1065-6995
- Publication type
Article
- DOI
10.1002/cbin.11236