Folch E, Prats N, Hotter G, López S, Gelpi E, Roselló-Catafau J, Closa D
Department of Medical Bioanalysis, Institut d'Investigacions Biomèdiques de Barcelona-Consejo Superior de Investigaciones Científicas, Spain.
Dig Dis Sci. 2000 Aug;45(8):1535-44. doi: 10.1023/a:1005552725243.
This work studied the activation of hepatic macrophages during acute pancreatitis and the involvement of these cells in the lung inflammatory response. Pancreatitis was induced in Wistar rats by intraductal administration of 5% sodium taurocholate. Three hours after pancreatitis induction, the degree of pulmonary inflammation, TNF-alpha levels, and P-selectin expression were evaluated. The generation of TNF-alpha by Kupffer cells was also measured. Pancreatitis increases the serum concentration of TNF-alpha, neutrophil infiltration, and P-selectin expression in pancreas and lung. In addition, Kupffer cells generate increased levels of TNF-alpha. When Kupffer cells were inhibited, the increase in serum TNF-alpha levels and the infiltration of neutrophils in the lung were prevented, but P-selectin expression remained unmodified. We conclude that pulmonary inflammation induced by acute pancreatitis is mediated by Kupffer cell activation and that pancreatitis induces the expression of P-selectin on pulmonary endothelial cells but this effect is not mediated by Kupffer cells.
本研究探讨了急性胰腺炎期间肝巨噬细胞的激活情况以及这些细胞在肺部炎症反应中的作用。通过向Wistar大鼠胰管内注射5%牛磺胆酸钠诱导胰腺炎。诱导胰腺炎3小时后，评估肺部炎症程度、肿瘤坏死因子-α（TNF-α）水平和P-选择素表达。同时检测库普弗细胞产生TNF-α的情况。胰腺炎会增加血清TNF-α浓度、中性粒细胞浸润以及胰腺和肺部的P-选择素表达。此外，库普弗细胞产生的TNF-α水平升高。当库普弗细胞受到抑制时，血清TNF-α水平的升高和肺部中性粒细胞浸润得到预防，但P-选择素表达未发生改变。我们得出结论，急性胰腺炎诱导的肺部炎症是由库普弗细胞激活介导的，胰腺炎诱导肺内皮细胞上P-选择素的表达，但这种作用不是由库普弗细胞介导的。
