Yang Jie, Yang Lin, Wang Yanjiao, Huai Lu, Shi Bohan, Zhang Di, Xu Wei, Cui Di
Department of Emergency, the People's Hospital of Liaoning Province, 33 Wenyi Road, Shenhe District, Shenyang, 110016, China.
Mol Med. 2025 Jan 31;31(1):34. doi: 10.1186/s10020-025-01089-6.
Sepsis is associated with immune dysregulated and organ dysfunction due to severe infection. Clinicians aim to restore organ function, rather than prevent diseases that are prone to sepsis, resulting in high mortality and a heavy public health burden. Some chronic diseases can induce sepsis through inflammation cascade reaction and Cytokine Storm (CS). Interleukin (IL)-6, the core of CS, and its related signaling pathways have been considered as contributors to sepsis. Therefore, it is important to study the relationship between IL-6 and its related pathways in sepsis-related chronic diseases. This review generalized the mechanism of sepsis-related chronic diseases via IL-6 related pathways with the purpose to take rational management for these diseases. IL-6 related signaling pathways were sought in Kyoto Encyclopedia of Genes and Genomes (KEGG), and retrieved protein-protein interaction in the Search for Interaction Genes tool (STRING). In PubMed and Google Scholar, the studies were searched out, which correlating to IL-6 related pathways and associating with the pathological process of sepsis. Focused on the interactions of sepsis and IL-6 related pathways, some chronic diseases have been studied for association with sepsis, containing insulin resistance, Alcoholic liver disease (ALD), Alzheimer disease (AD), and atherosclerosis. This article summarized the inflammatory mechanisms of IL-6 cross-talked with other mediators of some chronic diseases in vitro, animal models, and human experiments, leading to the activation of pathways and accelerating the progression of sepsis. The clinicians should be highlight to this kind of diseases and more clinical trials are needed to provide more reliable theoretical basis for health policy formulation.
脓毒症与严重感染导致的免疫失调和器官功能障碍有关。临床医生旨在恢复器官功能,而非预防易引发脓毒症的疾病,这导致了高死亡率和沉重的公共卫生负担。一些慢性疾病可通过炎症级联反应和细胞因子风暴(CS)诱发脓毒症。白细胞介素(IL)-6是CS的核心,其相关信号通路被认为是脓毒症的促成因素。因此,研究脓毒症相关慢性疾病中IL-6与其相关通路之间的关系具有重要意义。本综述通过IL-6相关通路概括了脓毒症相关慢性疾病的机制,旨在对这些疾病进行合理管理。在京都基因与基因组百科全书(KEGG)中查找IL-6相关信号通路,并在搜索相互作用基因工具(STRING)中检索蛋白质-蛋白质相互作用。在PubMed和谷歌学术中搜索与IL-6相关通路相关且与脓毒症病理过程相关的研究。聚焦于脓毒症与IL-6相关通路的相互作用,对一些与脓毒症相关的慢性疾病进行了研究,包括胰岛素抵抗、酒精性肝病(ALD)、阿尔茨海默病(AD)和动脉粥样硬化。本文总结了在体外、动物模型和人体实验中IL-6与一些慢性疾病的其他介质相互作用的炎症机制,导致通路激活并加速脓毒症进展。临床医生应重视这类疾病,需要更多的临床试验为卫生政策制定提供更可靠的理论依据。