Analysis of pathophysiology in acute pancreatitis from the stand point of CARS

从CARS角度分析急性胰腺炎的病理生理学

• 批准号: 13470242
• 负责人: OGAWA Michio
• 金额: $ 8.26万
• 依托单位: Kumamoto University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 2001
• 资助国家: 日本
• 起止时间: 2001 至 2002
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-13470242/
• 关键词: acute pancreatitis; CARS; cytokine antagonist; organ dysfunction; infection; cytokine; サイトカイン拮抗物質; 遠隔臓器障害; 重症急性膵炎; SIRS; 敗血症; 臓器障害; 好中球

Acute pancreatitis is a potentially fatal disease. Most patients develop systemic inflammatory response syndrome (SIRS), which is induced by inflammatory cytokines. Alternatively, patients with severe inflammatory insults also undergo an anti-inflammatory phase, the compensatory anti-inflammatory response syndrome (CARS). This condition is characterized by the production of cytokine antagonists and, as a result, suppression of cytokine response, which may result in immune suppression. In this project, we analyzed acute pancreatitis from the viewpoints of CARS.We elucidated the following points with this study, 1) In acute pancreatitis, abundant a mount cytokine antagonist is produced. 2) In the anaphase of the disease, de novo production of cytokines is suppressed by the cytokine antagonists. 3) Endotoxin can stimulate neutrophils accumulated in the distant organs to produce neutrophil elastase and reactive oxygen, and, as a result, provoke distant organ destruction without de novo cytokine production.

急性胰腺炎是一种潜在的致命性疾病。大多数患者发生全身炎症反应综合征（SIRS），这是由炎性细胞因子引起的。或者，患有严重炎性损伤的患者也经历抗炎阶段，即代偿性抗炎反应综合征（汽车）。这种病症的特征在于产生细胞因子拮抗剂，并因此抑制细胞因子应答，这可能导致免疫抑制。本课题从汽车的角度对急性胰腺炎进行了分析，阐明了以下几点：1）急性胰腺炎产生大量的细胞因子拮抗剂; 2)在疾病的后期，细胞因子的从头产生被细胞因子拮抗剂抑制。3)内毒素可刺激积聚在远端器官中的中性粒细胞产生中性粒细胞弹性蛋白酶和活性氧，因此，引起远端器官破坏而不重新产生细胞因子。

项目成果

Hirota M. et al.: "Visualization of the heterogeneous internal structure of so-called "pancreatic necrosis" by magnetic resonance imaging in acute necrotizing pancreatitis"Pancreas. 25. 63-67 (2002)

Hirota M. 等人：“通过磁共振成像对急性坏死性胰腺炎中所谓的‘胰腺坏死’的异质内部结构进行可视化”。

Okabe A, et al.: "Altered cytokine response in rat acute pancreatits complicated with endotoxemia"Pancreas. 22. 32-39 (2001)

Okabe A 等人：“大鼠急性胰腺炎并发内毒素血症时细胞因子反应的改变”胰腺。

Ogawa M.: "From SIRS and CARS to SLIRS and LISIS -new concepts for understanding the development of organ failure after clinical insults"Clin Intersivc Care. 13. 143-146 (2002)

小川 M.：“从 SIRS 和 CARS 到 SLIRS 和 LISIS - 了解临床损伤后器官衰竭发展的新概念”Clin Intersivc Care。

Hirota M, Kamekawa K, Tashima T, Mizumoto M, Ohara C, Beppu T, Shimada S, Yamaguchi Y, Ogawa M: "Percutaneous embolization of the distal pancreatic duct to treat intractable pancreatic juice fistula."Pancreas. 22. 214-216 (2001)

Hirota M，Kamekawa K，Tashima T，Mizumoto M，Ohara C，Beppu T，Shimada S，Yamaguchi Y，Okawa M：“经皮远端胰管栓塞治疗顽固性胰液瘘。”胰腺。

Kuwata K, Hirota M, Sugita H, Kai M, Hayashi N, Nakamura M, Matsubara T, Adachi N, Nishimori I, Ogawa M: "Genetic mutations in exon 3 and 4 of pancreatic secretory trypsin inhibitor in patients with pancreatitis."J Gastroenterol. 36. 612-618 (2001)

Kuwata K、Hirota M、Sugita H、Kai M、Hayashi N、Nakamura M、Matsubara T、Adachi N、Nishimori I、Okawa M：“胰腺炎患者胰腺分泌性胰蛋白酶抑制剂外显子 3 和 4 的基因突变。”J