Abstract
Previous studies show that long noncoding RNA intersectin 1-2 (lnc-ITSN1-2) promotes the inflammation process and serves as a potential biomarker in autoimmune diseases, except for ankylosing spondylitis (AS). Therefore, this study aimed to explore the correlation of baseline lnc-ITSN1-2 expression with disease risk and activity of AS, and to investigate its longitudinal change with treatment response to a tumour necrosis factor alpha (TNFα) inhibitor in patients with AS. In total, 63 patients with AS receiving 12-week adalimumab treatment were included and their baseline clinical features were collected. Lnc-ITSN1-2 expression in peripheral blood mononuclear cells (PBMC) of patients with AS was detected by reverse transcription quantitative polymerase chain reaction. Meanwhile, Assessment in Spondyloarthritis International Society (ASAS) 40 response was evaluated at week 2 (W2), W4, W8, and W12. According to the ASAS40 response status at W12, patients with AS were classified into responders and non-responders. PBMC lnc-ITSN1-2 expression was also determined in healthy controls (N = 60). Lnc-ITSN1-2 expression was elevated in patients with AS compared to controls (P < 0.001). Baseline lnc-ITSN1-2 expression was positively associated with C-reaction protein (CRP) (P = 0.021), interleukin (IL)-1β (P = 0.020), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) score (P = 0.040), and Ankylosing Spondylitis Disease Activity score with C-reactive protein (ASDASCRP) (P = 0.045) in patients with AS. Furthermore, lnc-ITSN1-2 expression declined during the treatment with adalimumab (P < 0.001). Notably, this reduction was more obvious in responders than non-responders. In conclusion, declined lnc-ITSN1-2 expression during the TNFα inhibitor treatment correlates with good treatment efficacy in patients with AS, suggesting its clinical value for AS management.
Highlights
Ankylosing spondylitis (AS) is a chronic inflammatory disease that mainly affects the axial skeleton with unknown etiology (Smith 2015)
Previous clinical studies show that lnc-ITSN1-2 expression is upregulated and its high expression correlates with elevated inflammation and increased disease activity reflected by DAS28 score in patients with rheumatoid arthritis (RA) (Gong et al 2017; Yue et al 2019). lncITSN1-2 expression correlates with disease risk and active disease status of inflammatory bowel disease (IBD), and it positively correlates with C-reaction protein (CRP), ESR, and Crohn’s disease activity index in patients with active Crohn’s disease (CD) (Nie and Zhao 2020)
We performed this study and discovered that lnc-ITSN1-2 expression was elevated in patients with ankylosing spondylitis (AS) compared to controls and it correlated with AS risk
Summary
Ankylosing spondylitis (AS) is a chronic inflammatory disease that mainly affects the axial skeleton with unknown etiology (Smith 2015). Lnc-ITSN1-2 may promote the differentiation of T helper type 1 (Th1) and Th17 cells in C D4+ T cells of inflammatory bowel disease (IBD) via regulating the microRNA (miR)-125a/interleukin (IL)23R axis (Nie and Zhao 2020). LncITSN1-2 expression correlates with RA risk and IBD risk, and it correlates with elevated disease activity in patients with RA and patients with IBD (Gong et al 2017; Nie and Zhao 2020; Yue et al 2019). Lnc-ITSN1-2 expression is reduced after the TNFα inhibitor treatment in patients with active IBD (Nie and Zhao 2020). We intended to investigate lnc-ITSN1-2 longitudinal change during the TNFα inhibitor (adalimumab) treatment and its association with treatment efficacy in patients with AS
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