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Ulcerative colitis: understanding its cellular pathology could provide insights into novel therapies.
Journal of Inflammation ( IF 4.4 ) Pub Date : 2020-04-21 , DOI: 10.1186/s12950-020-00246-4
Amandip Kaur 1 , Paraskevi Goggolidou 1
Affiliation  

Dynamic interactions between the gastrointestinal epithelium and the mucosal immune system normally contribute to ensuring intestinal homeostasis and optimal immunosurveillance, but destabilisation of these interactions in genetically predisposed individuals can lead to the development of chronic inflammatory diseases. Ulcerative colitis is one of the main types of inflammatory diseases that affect the bowel, but its pathogenesis has yet to be completely defined. Several genetic factors and other inflammation-related genes are implicated in mediating the inflammation and development of the disease. Some susceptibility loci associated with increased risk of ulcerative colitis are found to be implicated in mucosal barrier function. Different biomarkers that cause damage to the colonic mucosa can be detected in patients, including perinuclear ANCA, which is also useful in distinguishing ulcerative colitis from other colitides. The choice of treatment for ulcerative colitis depends on disease severity. Therapeutic strategies include anti-tumour necrosis factor alpha (TNF-α) monoclonal antibodies used to block the production of TNF-α that mediates intestinal tract inflammation, an anti-adhesion drug that prevents lymphocyte infiltration from the blood into the inflamed gut, inhibitors of JAK1 and JAK3 that suppress the innate immune cell signalling and interferons α/β which stimulate the production of anti-inflammatory cytokines, as well as faecal microbiota transplantation. Although further research is still required to fully dissect the pathophysiology of ulcerative colitis, understanding its cellular pathology and molecular mechanisms has already proven beneficial and it has got the potential to identify further novel, effective targets for therapy and reduce the burden of this chronic disease.

中文翻译:

溃疡性结肠炎:了解其细胞病理学可以提供新疗法的见解。

胃肠道上皮和粘膜免疫系统之间的动态相互作用通常有助于确保肠内稳态和最佳的免疫监视,但是在遗传易感人群中,这些相互作用的不稳定会导致慢性炎症性疾病的发展。溃疡性结肠炎是影响肠的主要炎性疾病之一,但其发病机理尚未完全阐明。几种遗传因素和其他与炎症有关的基因与介导疾病的炎症和发展有关。发现与溃疡性结肠炎风险增加相关的一些易感基因座与粘膜屏障功能有关。可以在患者中检测到导致结肠粘膜受损的不同生物标志物,包括核周ANCA,这也有助于区分溃疡性结肠炎与其他大肠菌群。溃疡性结肠炎的治疗选择取决于疾病的严重程度。治疗策略包括用于阻止介导肠道炎症的TNF-α产生的抗肿瘤坏死因子α(TNF-α)单克隆抗体,一种防止淋巴细胞从血液浸入发炎的肠道的抗粘连药物,抑制先天免疫细胞信号传导的JAK1和JAK3和刺激抗炎细胞因子以及粪便微生物群移植的干扰素α/β。尽管仍需要进一步研究以充分剖析溃疡性结肠炎的病理生理,
更新日期:2020-04-22
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