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Proposed protective mechanism of the pancreas in the rat

机译：拟议的大鼠胰腺保护机制

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Background Heparan sulphate is known to have various functions in the animal body, including surveillance of tissue integrity. Administered intraperitoneally, it induces a systemic inflammatory response syndrome and when given locally in the pancreas it initiates a protective inflammatory response. The aim of the present study was to investigate the underlying mechanisms behind cell recruitment following intra-ductal infusion of heparan sulphate. Methods Rats were subjected to intraductal-infusion of heparan sulphate, lipopolysaccharide and phosphate buffered saline into the pancreas. Pancreatic tissue was harvested 1, 3, 6, 9 or 48 hours after infusion and stained immunohistochemically for myeloperoxidase, ED-1, CINC-1 and MCP-1, as well as using eosin hematoxylin staining. Furthermore, MPO activity and MCP-1 and CINC-1 concentrations of tissue homogenates were measured. All differences were analyzed statistically using the Mann-Whitney U-test. Results During HS infusion, a rapid influx of macrophages/monocytes, as visualized as ED-1 positive cells, was seen reaching a maximum at 6 hours. After 48 hours, the same levels of ED-1 positive cells were noted in the pancreatic tissue, but with different location and morphology. Increased neutrophil numbers of heparan sulphate treated animals compared to control could be detected only 9 hours after infusion. The number of neutrophils was lower than the number of ED-1 positive cells. On the contrary, LPS infusion caused increased neutrophil numbers to a larger extent than heparan sulphate. Furthermore, this accumulation of neutrophils preceded the infiltration of ED-1 positive cells. Chemokine expression correlates very well to the cell infiltrate. MCP-1 was evident in the ductal cells of both groups early on. MCP-1 preceded monocyte infiltration in both groups, while the CINC-1 increase was only noticeable in the LPS group. Conclusions Our data suggest that heparan and LPS both induce host defense reactions, though by using different mechanisms of cell-recruitment. This implies that the etiology of pancreatic inflammation may influence how the subsequent events will develop.
机译：背景技术已知硫酸乙酰肝素在动物体内具有多种功能，包括监视组织完整性。腹膜内给药可诱发全身性炎症反应综合征，胰腺局部给予时可引发保护性炎症反应。本研究的目的是研究导管内输注硫酸乙酰肝素后细胞募集的潜在机制。方法对大鼠胰管内注入硫酸乙酰肝素，脂多糖和磷酸盐缓冲液。输注后1、3、6、9或48小时收集胰腺组织，并用免疫组织化学方法对髓过氧化物酶，ED-1，CINC-1和MCP-1进行染色，并使用曙红苏木精染色。此外，测量了MPO活性以及组织匀浆的MCP-1和CINC-1浓度。使用Mann-Whitney U检验对所有差异进行统计学分析。结果在HS输注过程中，可以看到巨噬细胞/单核细胞快速流入，如ED-1阳性细胞所示，在6小时时达到最大值。 48小时后，在胰腺组织中观察到相同水平的ED-1阳性细胞，但是具有不同的位置和形态。与对照组相比，硫酸乙酰肝素处理的动物的嗜中性粒细胞数量增加，仅在输注后9小时即可检测到。中性粒细胞的数量低于ED-1阳性细胞的数量。相反，与硫酸乙酰肝素相比，LPS输注引起的中性粒细胞数量增加更大。此外，嗜中性粒细胞的这种积累先于ED-1阳性细胞的浸润。趋化因子表达与细胞浸润非常相关。早期，两组的导管细胞中均存在MCP-1。在两组中，MCP-1都在单核细胞浸润之前，而仅在LPS组中，CINC-1的增加才明显。结论我们的数据表明，尽管通过使用不同的细胞招募机制，肝素和LPS均可诱导宿主防御反应。这意味着胰腺炎症的病因可能会影响后续事件的发展。

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