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Background: This work aimed to explore anxiety-associated risk factors in patients diagnosed with ulcerative colitis (UC). Methods: Clinical data from patients diagnosed with UC and hospitalized at the First Affiliated Hospital of Xi'an Jiaotong University between May 2019 and June 2022 were retrospectively analyzed. A total of 260 patients were included and divided into UC with anxiety (n = 86) and UC without anxiety (n = 174) groups according to the Self-Rating Anxiety Scale score. The quality of life and disease activity in patients with UC were assessed using the Inflammatory Bowel Disease Questionnaire and Mayo Score, respectively. Clinical data, disease characteristics, quality of life, disease activity, and noise exposure were compared between the groups, and factors contributing to anxiety in patients with UC were explored through multivariate logistic regression analysis. Results: No significant difference was found between the groups in terms of disease duration (P = 0.73), distribution of disease (P = 0.86), or medication use (P = 0.86). However, compared to UC patients without anxiety, those with anxiety were older (P < 0.05), predominantly female (P < 0.05), had lower quality of life (P < 0.05), experienced higher disease activity (P < 0.05), and had greater noise exposure (P < 0.05). The quality of life [odds ratio (OR) = 0.558, 95% confidence interval (CI) = 0.348–0.895, P = 0.02] was a protective factor for anxiety in patients with UC. Disease activity (OR = 1.680, 95% CI = 1.103–2.561, P = 0.02) and noise exposure (OR = 2.148, 95% CI = 1.084–4.106, P = 0.01) were significant risk factors for anxiety in patients with UC. Conclusion: Noise exposure and disease activity were associated with an increased risk of anxiety in patients with UC, whereas higher quality of life was protective against anxiety in UC patients. [ABSTRACT FROM AUTHOR]

The corticotropin-releasing factor (CRF) family is involved in modulating gastrointestinal motility, sensitivity and inflammation. CRF signalling exerts an important role in inflammatory bowel disease (IBD), predominantly by activating CRF receptors. The aim of the present study was to investigate the function of CRF receptor 1 (CRF-R1) in the development of mucosal inflammation induced by dextran sulphate sodium (DSS) and the underlying mechanism. Consecutive administration of CRF or CP154526 was used to activate or block the CRF-R1 in DSS-treated mice. Colonic inflammation was evaluated by determining the Disease Activity Index (DAI) and histology score. CRF-R1 expression was proportional to the DAI, the histology score and the number of macrophages. Activation of CRF-R1 aggravated mucosal inflammation by activating nuclear factor (NF)-κB and subsequently increasing the expression levels of tumour necrosis factor (TNF)-α and interleukin (IL)-6. Inhibition of CRF-R1 decreased the expression level of CRF-R1, macrophage infiltration, NF-κB activation, and TNF-α and IL-6 expression levels, ultimately alleviating the mucosal inflammation. Thus, CRF-R1 expression was proportional to the severity of DSS-induced colitis. Activation of CRF-R1 increased the DAI and histological scores of the colons from DSS-treated mice by promoting M1 macrophage polarization, demonstrated as increased NF-κB activation, and TNF-α and IL-6 release. These results provide evidence of the pro-inflammatory role of CRF-R1 in a DSS-induced ulcerative colitis (UC) model and a possible underlying mechanism, which may facilitate the elucidation of potential treatment approaches for UC. [ABSTRACT FROM AUTHOR]