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急性胰腺炎中细胞坏死的循环标志物。

Circulating Markers of Necroptosis in Acute Pancreatitis.

机构信息

Department of Surgery, Helsinki University Hospital and University of Helsinki, Haartmaninkatu 4, 00290, Helsinki, Finland.

Department of Bacteriology and Immunology, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.

出版信息

Dig Dis Sci. 2024 Sep;69(9):3333-3343. doi: 10.1007/s10620-024-08530-6. Epub 2024 Jun 28.

DOI:10.1007/s10620-024-08530-6
PMID:38940973
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11415434/
Abstract

OBJECTIVES

Necroptosis, a programmed inflammatory cell death, is involved in the pathogenesis of acute pancreatitis (AP). We compared levels of interleukin (IL)-33 (released upon necroptosis), sST2 (soluble IL-33 receptor), MLKL, RIPK1 and RIPK3 (necroptosis executioner proteins), and proinflammatory cytokines IL-6, TNF and IL-1β at various severity categories and stages of AP.

METHODS

Plasma from 20 patients with early mild AP (MAP) (symptom onset < 72 h), 7 with severe AP (SAP) without and 4 with persistent organ failure (OF) at sampling, 8 patients with late SAP and 20 healthy controls (HC) were studied by ELISAs.

RESULTS

Early sST2 and IL-6 levels predicted the development of SAP and were higher in both MAP and early and late SAP than in HC. RIPK3 levels were higher than in HC in the patients who had or would later have SAP. MLKL levels were associated with the presence of OFs, particularly in the late phase, but were also higher in MAP than in HC.

CONCLUSIONS

sST2, RIPK3 and IL-6 levels may have prognostic value in AP. Elevated MLKL levels are associated with OF in AP. Better understanding of necroptosis in AP pathophysiology is needed to evaluate whether inhibiting and targeting necroptosis is a potential therapeutic option in AP.

摘要

目的

细胞程序性坏死（坏死性凋亡）参与了急性胰腺炎（AP）的发病机制。我们比较了不同严重程度分类和 AP 不同阶段中白细胞介素（IL）-33（坏死性凋亡时释放）、sST2（IL-33 可溶性受体）、MLKL、RIPK1 和 RIPK3（坏死性凋亡执行蛋白）以及促炎细胞因子 IL-6、TNF 和 IL-1β的水平。

方法

通过 ELISA 法检测了 20 例早期轻度 AP（MAP）（症状发作<72 小时）患者、7 例 SAP 患者（无持续性器官衰竭）和 4 例 SAP 患者（在采样时发生持续性器官衰竭）、8 例晚期 SAP 患者和 20 例健康对照者（HC）的血浆样本。

结果

早期 sST2 和 IL-6 水平预测 SAP 的发生，且在 MAP 及早期和晚期 SAP 患者中均高于 HC。RIPK3 水平在 SAP 患者（无论是否发生）中均高于 HC。MLKL 水平与 OFs 的存在相关，尤其是在晚期阶段，但在 MAP 患者中也高于 HC。

结论

sST2、RIPK3 和 IL-6 水平可能对 AP 具有预后价值。AP 中 MLKL 水平升高与 OF 相关。为了评估抑制和靶向坏死性凋亡是否是 AP 的一种潜在治疗选择，需要更好地了解 AP 病理生理学中的坏死性凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d81b/11415434/ab37bb50e115/10620_2024_8530_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d81b/11415434/be7a723c2399/10620_2024_8530_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d81b/11415434/c465f33aa68f/10620_2024_8530_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d81b/11415434/ab37bb50e115/10620_2024_8530_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d81b/11415434/be7a723c2399/10620_2024_8530_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d81b/11415434/c465f33aa68f/10620_2024_8530_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d81b/11415434/ab37bb50e115/10620_2024_8530_Fig3_HTML.jpg

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本文引用的文献

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Soluble ST2 as a New Oxidative Stress and Inflammation Marker in Metabolic Syndrome.可溶性 ST2 作为代谢综合征中新的氧化应激和炎症标志物。
Int J Environ Res Public Health. 2023 Jan 31;20(3):2579. doi: 10.3390/ijerph20032579.
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Blood Leukocyte Signaling Pathways as Predictors of Severity of Acute Pancreatitis.血液白细胞信号通路作为急性胰腺炎严重程度的预测指标。
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Occurrence and Risk Factors of Infected Pancreatic Necrosis in Intensive Care Unit-Treated Patients with Necrotizing Severe Acute Pancreatitis.
重症监护病房治疗的坏死性重症急性胰腺炎患者感染性胰腺坏死的发生和危险因素。
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Protective effect of necrosulfonamide on rat pulmonary ischemia-reperfusion injury via inhibition of necroptosis.通过抑制坏死性凋亡，烟酰胺对大鼠肺缺血再灌注损伤的保护作用。
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Circulating Receptor-Interacting Protein Kinase 3 Are Increased in HBV Patients With Acute-on-Chronic Liver Failure and Are Associated With Clinical Outcome.循环受体相互作用蛋白激酶3在慢性乙型肝炎急性肝衰竭患者中升高，并与临床结局相关。
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Soluble ST2 promotes oxidative stress and inflammation in cardiac fibroblasts: an and study in aortic stenosis.可溶性 ST2 在心脏成纤维细胞中促进氧化应激和炎症：一项主动脉瓣狭窄的体内和体外研究。
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Necroptosis directly induces the release of full-length biologically active IL-33 in vitro and in an inflammatory disease model.体外和炎症性疾病模型中，坏死性凋亡直接诱导全长生物活性的 IL-33 释放。
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