Hammad Dargham, Muslim Alameedy Fadyia Mahdi
Department of Pathological Analysis, Faculty of Science, Kufa University, Najaf, Iraq.
Middle East J Dig Dis. 2024 Jul;16(3):185-192. doi: 10.34172/mejdd.2024.388. Epub 2024 Jul 31.
The current research examines the molecular terrain of celiac disease (CD) through microRNA (miRNA) and cytokines as potential new diagnostic and therapeutic markers. Gluten-appropriate immune response is a key feature of an autoimmune clinical entity known as CD that leads to inflammation and degeneration of small intestine mucosa. However, the mechanisms responsible for this remain unclear.
Quantitative reverse transcription polymerase chain reaction (RT-qPCR ) was carried out on serum samples obtained from patients with CD and control groups to unravel their pathogenesis. Assessing miR-155, miR-15b, interleukin (IL)-2, IL-7, IL-35and IL-37 levels in expression might be useful in diagnosing or treating the disorder.
A significant dysregulation of these molecular players in patients with CD compared with healthy controls has been evidenced by results from this study. For instance, miR-155 was up-regulated, whereas miR-15b was significantly down-regulated in CD, illustrating their roles in immune responses and inflammation-mediated processes. Besides, there was an over-expression of IL-2 and an under-expression of IL-37 in patients with CD, indicating these biomolecules' role in immuno-dysregulation and inflammatory process underlying CD. In addition, a positive correlation between IL-2 and miRNA 155 expression levels was observed in patients with CD, suggesting that they could be involved together with other cytokines, showing the interplay between immune response pathways and inflammatory cascades during CD pathogenesis.
These molecular signature discoveries might result in new and revolutionary diagnostic modalities and molecular-targeted therapies for CD pathogenesis. When used with the scientific understanding of miRNAs and cytokines associated with CD pathophysiology, it creates a basis for personalized medicine based on the individualized molecular profile of all patients. This will undoubtedly increase the efficacy of CD treatment strategies. In brief, more research on molecular pathways' workings should be done to harness their potential in CD diagnosis and treatment.
当前研究通过微小RNA(miRNA)和细胞因子来探究乳糜泻(CD)的分子机制,将其作为潜在的新型诊断和治疗标志物。对麸质产生适当的免疫反应是一种名为乳糜泻的自身免疫性临床疾病的关键特征,该疾病会导致小肠黏膜发生炎症和退化。然而,其发病机制尚不清楚。
对来自CD患者和对照组的血清样本进行定量逆转录聚合酶链反应(RT-qPCR),以揭示其发病机制。评估miR-155、miR-15b、白细胞介素(IL)-2、IL-7、IL-35和IL-37的表达水平可能有助于诊断或治疗该疾病。
本研究结果表明,与健康对照组相比,CD患者中这些分子成分存在明显的失调。例如,miR-155在CD中上调,而miR-15b则显著下调,这说明了它们在免疫反应和炎症介导过程中的作用。此外,CD患者中IL-2过表达,IL-37表达不足,表明这些生物分子在CD潜在的免疫失调和炎症过程中发挥作用。此外,在CD患者中观察到IL-2与miRNA 155表达水平之间呈正相关,这表明它们可能与其他细胞因子共同参与其中,显示了CD发病机制中免疫反应途径与炎症级联反应之间的相互作用。
这些分子特征的发现可能会为CD发病机制带来新的、革命性的诊断方法和分子靶向治疗。当与对与CD病理生理学相关的miRNA和细胞因子的科学理解相结合时,它为基于所有患者个体化分子特征的个性化医疗奠定了基础。这无疑将提高CD治疗策略的疗效。简而言之,应进一步研究分子途径的作用机制,以挖掘它们在CD诊断和治疗中的潜力。