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首页> 外文期刊>Journal of Cellular Physiology >The calcium binding protein S100A9 is essential for pancreatic leukocyte infiltration and induces disruption of cell-cell contacts.
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The calcium binding protein S100A9 is essential for pancreatic leukocyte infiltration and induces disruption of cell-cell contacts.

机译：钙结合蛋白S100A9是至关重要的胰腺白细胞浸润和诱导中断的信息联系。

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摘要

Leukocyte infiltration is an early and critical event in the development of acute pancreatitis. However, the mechanism of leukocyte transmigration into the pancreas and the function of leukocytes in initiating acute pancreatitis are still poorly understood. Here, we studied the role of S100A9 (MRP14), a calcium binding protein specifically released by polymorph nuclear leukocytes (PMN), in the course of acute experimental pancreatitis. Acute pancreatitis was induced by repeated supramaximal caerulein injections in S100A9 deficient or S100A9 wild-type mice. We then determined S100A9 expression, trypsinogen activation peptide (TAP) levels, serum amylase and lipase activities, and tissue myeloperoxidase (MPO) activity. Cell-cell contact dissociation was analyzed in vitro with biovolume measurements of isolated acini after incubation with purified S100A8/A9 heterodimers, and in vivo as measurement of Evans Blue extravasation after intravenous application of S100A8/A9. Pancreatitis induced increased levels of S100A9 in the pancreas. However, infiltration of leukocytes and MPO activity in the lungs and pancreas during acute pancreatitis was decreased in S100A9-deficient mice and associated with significantly lower serum amylase and lipase activities as well as reduced intrapancreatic TAP-levels. Incubation of isolated pancreatic acini with purified S100A8/A9-heterodimers resulted in a rapid dissociation of acinar cell-cell contacts which was highly calcium-dependent. Consistent with these findings, in vivo application of S100A8/A9 in mice was in itself sufficient to induce pancreatic cell-cell contract dissociation as indicated by Evans Blue extravasation. These data show that the degree of intrapancreatic trypsinogen activation is influenced by the extent of leukocyte infiltration into the pancreas which, in turn, depends on the presence of S100A9 that is secreted from PMN. S100A9 directly affects leukocyte tissue invasion and mediates cell contact dissociation via its calcium binding properties.
机译：白细胞浸润是一个早期和至关重要的在急性胰腺炎的发展。然而,白细胞的机制轮回成胰腺和函数引发急性胰腺炎的白细胞仍然知之甚少。S100A9角色(MRP14),钙结合蛋白专门发布的变形核白细胞(中性粒细胞),过程中严重实验胰腺炎。引起重复超大的caerulein注射S100A9不足或S100A9野生型老鼠。表情,胰蛋白酶原激活肽(TAP)水平,血清淀粉酶和脂肪酶的活动,组织髓过氧化酶(MPO)活动。接触分离分析了体外biovolume测量后的孤立的腺泡孵化与纯化S100A8 / A9形成,伊文思蓝的和体内测量外渗后静脉应用S100A8 / A9。S100A9的胰腺。在肺部和白细胞和MPO的活动在急性胰腺炎胰腺下降在S100A9-deficient老鼠和相关联的显著降低血清淀粉酶和脂肪酶以及减少胰腺内的活动TAP-levels。腺泡和纯化S100A8 / A9-heterodimers导致腺泡的的快速分离信息接触高度calcium-dependent。发现,体内S100A8 / A9的应用老鼠本身就是足够的诱导胰腺和信息合同离解由伊文思蓝表示溢出。显示的程度内胰蛋白酶原激活的影响白细胞浸润的程度反过来,胰腺,取决于存在从中性粒细胞的S100A9分泌。直接影响组织入侵和白细胞通过其介导细胞接触分离钙绑定属性。

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