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抗炎细胞因子:有助于化疗诱导的胃肠道粘膜炎的重要免疫调节因子。

Anti-inflammatory cytokines: important immunoregulatory factors contributing to chemotherapy-induced gastrointestinal mucositis.

作者信息

Sultani Masooma, Stringer Andrea M, Bowen Joanne M, Gibson Rachel J

机构信息

School of Medical Sciences, University of Adelaide, North Terrace, Adelaide, SA 5005, Australia.

出版信息

Chemother Res Pract. 2012;2012:490804. doi: 10.1155/2012/490804. Epub 2012 Sep 2.

Abstract

"Mucositis" is the clinical term used to describe ulceration and damage of the mucous membranes of the entire gastrointestinal tract (GIT) following cytotoxic cancer chemotherapy and radiation therapy common symptoms include abdominal pain, bloating, diarrhoea, vomiting, and constipation resulting in both a significant clinical and financial burden. Chemotherapeutic drugs cause upregulation of stress response genes including NFκB, that in turn upregulate the production of proinflammatory cytokines such as interleukin-1β (IL-1β), Interleukin-6 (IL-6), and tumour necrosis factor-α (TNF-α). These proinflammatory cytokines are responsible for initiating inflammation in response to tissue injury. Anti-inflammatory cytokines and specific cytokine inhibitors are also released to limit the sustained or excessive inflammatory reactions. In the past decade, intensive research has determined the role of proinflammatory cytokines in development of mucositis. However, a large gap remains in the knowledge of the role of anti-inflammatory cytokines in the setting of chemotherapy-induced mucositis. This critical paper will highlight current literature available relating to what is known regarding the development of mucositis, including the molecular mechanisms involved in inducing inflammation particularly with respect to the role of proinflammatory cytokines, as well as provide a detailed discussion of why it is essential to consider extensive research in the role of anti-inflammatory cytokines in chemotherapy-induced mucositis so that effective targeted treatment strategies can be developed.

摘要

“黏膜炎”是一个临床术语,用于描述细胞毒性癌症化疗和放射治疗后整个胃肠道(GIT)黏膜的溃疡和损伤。常见症状包括腹痛、腹胀、腹泻、呕吐和便秘,这会造成重大的临床和经济负担。化疗药物会导致包括核因子κB(NFκB)在内的应激反应基因上调,进而上调促炎细胞因子如白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的产生。这些促炎细胞因子负责在组织损伤时引发炎症。抗炎细胞因子和特定的细胞因子抑制剂也会释放出来,以限制持续或过度的炎症反应。在过去十年中,深入研究已经确定了促炎细胞因子在黏膜炎发展中的作用。然而,对于抗炎细胞因子在化疗诱导的黏膜炎中的作用,我们的认识仍存在很大差距。这篇重要论文将重点介绍当前有关黏膜炎发展的已知文献,包括诱导炎症的分子机制,特别是促炎细胞因子的作用,并详细讨论为什么必须深入研究抗炎细胞因子在化疗诱导的黏膜炎中的作用,以便制定有效的靶向治疗策略。

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