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Cell division control 42 elevates during infliximab therapy, and its increment relates to treatment response in ulcerative colitis patients
Author(s) -
Liu Lin,
Liu Qinger,
Chang Jian,
Dong Xiaoxia,
Ma Weiping
Publication year - 2022
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.24477
Subject(s) - medicine , ulcerative colitis , infliximab , gastroenterology , peripheral blood mononuclear cell , cdc42 , immunology , tumor necrosis factor alpha , disease , cell , biochemistry , chemistry , in vitro , genetics , biology
Background Cell division control 42 (CDC42) regulates multiple processes of inflammation and/or immunity in autoimmune diseases and also relates to the treatment efficacy of biologic regimens clinically. This study aimed to explore the longitudinal change in CDC42 during infliximab (IFX) treatment and its correlation with IFX response in ulcerative colitis (UC) patients. Methods Active UC patients ( N  = 48) who received IFX were recruited, and their CDC42 expressions in peripheral blood mononuclear cells (PBMCs) were detected before treatment (W0) and at 12 weeks after treatment (W12) using RT‐qPCR. Also, CDC42 in PBMCs from UC patients with remission ( N  = 20) and health controls (HCs) ( N  = 20) were detected. Results CDC42 was reduced in active UC patients compared with UC patients with remission ( p  = 0.014) and HCs ( p  < 0.001). Besides, CDC42 was negatively correlated with CRP ( p  = 0.025), TNF‐α ( p  = 0.024), IL‐1β ( p  = 0.045), IL‐17A ( p  = 0.039), and Mayo score ( p  = 0.015) in active UC patients, but did not relate to ESR, disease duration, or IL‐6 (all p  > 0.05), while CDC42 was only negatively related to CRP in UC patients with remission ( p  = 0.046). Interestingly, CDC42 was increased at W12 after IFX treatment in active UC patients ( p  < 0.001). Specifically, CDC42 was elevated during treatment in active UC patients with IFX response ( p  < 0.001), but did not obviously change in those without IFX response ( p  = 0.061). Furthermore, CDC42 at W12 was higher in active UC patients with IFX response compared with those without IFX response ( p  = 0.049). Conclusion Cell division control 42 serves as a potential biomarker for monitoring disease progression and IFX response in UC patients.

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