Department of Pharmaceutical Sciences, Babasaheb Bhimrao Ambedkar University, Vidya Vihar, Raebareli Road, Lucknow 226025, U.P., India.
Department of Pharmaceutical Sciences, Babasaheb Bhimrao Ambedkar University, Vidya Vihar, Raebareli Road, Lucknow 226025, U.P., India.
Int Immunopharmacol. 2023 Dec;125(Pt A):111046. doi: 10.1016/j.intimp.2023.111046. Epub 2023 Oct 23.
The global incidence of autoimmune diseases is on the rise, and many healthcare professionals believe that chronic stress plays a prominent role in both the aggravation and remission of these conditions. It is believed that prolonged exposure to stress is associated with neuroimmune axis malfunction, which eventually dysregulates multiple immunological factors as well as deregulates autoimmune responses that play a central role in various autoimmune diseases, including rheumatoid arthritis and psoriasis. Herein, we performed validation of an 8-week long rat model of chronic unpredictable stress (CUS) which consisted of exposing groups of rats to random stressors daily for 8 weeks. Additionally, we developed a novel rat model combining 8-week long random stressor-induced CUS with CIA-triggered arthritis and IMQ-triggered psoriasis and have successfully used both these models to assess the role of chronic stress in the aggravation of arthritis and psoriasis, respectively. Notably, the 8-week CUS protocol extensively aggravated and prolonged both arthritis and psoriasis condition in the rat model by upregulating the release of different pro-inflammatory cytokines, dysregulation of immune cell responses and oxidative stress system, which were all related to severe inflammation. Further, CUS aggravated macroscopic features and the increase in destruction of joint tissue and epidermal thickness induced by CIA and IMQ, respectively, in rats. In conclusion, this study suggests that exposure to an 8-week long CUS paradigm aggravates the distinctive characteristics of rheumatoid arthritis and psoriasis in rats via amplifying the inflammatory circuits and immune cell responses linked to these autoimmune diseases.
自身免疫性疾病的全球发病率呈上升趋势,许多医疗保健专业人员认为,慢性压力在这些疾病的恶化和缓解中起着突出的作用。人们认为,长期暴露于压力与神经免疫轴功能障碍有关,这最终会使多种免疫因子失调,并使自身免疫反应失控,而自身免疫反应在包括类风湿关节炎和银屑病在内的各种自身免疫性疾病中起着核心作用。在此,我们对为期 8 周的慢性不可预测性应激(CUS)大鼠模型进行了验证,该模型包括每天使大鼠暴露于随机应激源中 8 周。此外,我们还开发了一种新的大鼠模型,将 8 周长的随机应激源诱导的 CUS 与 CIA 诱导的关节炎和 IMQ 诱导的银屑病相结合,并成功地使用这两种模型来评估慢性应激在关节炎和银屑病恶化中的作用。值得注意的是,8 周的 CUS 方案通过上调不同促炎细胞因子的释放、免疫细胞反应和氧化应激系统的失调,广泛加重和延长了大鼠模型中的关节炎和银屑病病情,这些都与严重炎症有关。此外,CUS 加重了 CIA 和 IMQ 分别在大鼠中引起的关节组织破坏和表皮厚度增加的宏观特征。总之,这项研究表明,暴露于 8 周长的 CUS 范式通过放大与这些自身免疫性疾病相关的炎症回路和免疫细胞反应,加重了大鼠类风湿关节炎和银屑病的特征性表现。