Dysregulated interleukin 11 in primary Sjogren's syndrome contributes to apoptosis of glandular epithelial cells

The purpose of this study was to explore the potential function of interleukin-11 (IL-11) in the pathogenesis of primary Sjogren'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.