Campbell W N, Ding X, Goldblum S E
Division of Infectious Diseases, Maryland Institute for Emergency Medical Services Systems, Baltimore.
Am J Physiol. 1992 Jul;263(1 Pt 1):L128-36. doi: 10.1152/ajplung.1992.263.1.L128.
Human recombinant interleukin-1 alpha (rIL-1 alpha) and -beta were studied to determine whether either could alter the permeability of bovine pulmonary artery endothelial cell monolayers. Endothelial cells were grown to confluence on filters mounted in chemotaxis chambers placed in wells. Barrier function of the monolayers was assessed by placing 14C-labeled bovine serum albumin ([14C]BSA) in the upper chamber and sampling the lower well for [14C]BSA. rIL-1 alpha induced a significant (P less than 0.01) dose- and time-dependent increase in transendothelial [14C]BSA flux. rIL-1 alpha exposures as brief as 30 min increased permeability, but the increased albumin transfer could not be demonstrated before 4 h after exposure. Exposures up to 6 h were reversible at 24 h. rIL-1 alpha induced significantly (P less than 0.01) greater increments in [14C]BSA flux than did equivalent exposures to rIL-1 beta. No important differences between bovine and human rIL-1 beta were demonstrated. Increased transendothelial flux could not be ascribed to either endothelial cytotoxicity or growth inhibition. There was no additive or synergistic relationship between rIL-1 alpha and human recombinant tumor necrosis factor-alpha. Our studies suggest that IL-1 alpha and -beta may play a role in the pathogenesis of pulmonary vascular leak.
研究了重组人白细胞介素-1α（rIL-1α）和白细胞介素-1β，以确定它们是否能改变牛肺动脉内皮细胞单层的通透性。将内皮细胞培养至汇合状态，使其附着在置于孔中的趋化性小室中的滤膜上。通过将14C标记的牛血清白蛋白（[14C]BSA）置于上室，并在下孔中采集[14C]BSA样本，来评估单层的屏障功能。rIL-1α引起跨内皮[14C]BSA通量显著（P<0.01）的剂量和时间依赖性增加。短至30分钟的rIL-1α暴露即可增加通透性，但在暴露后4小时之前无法证明白蛋白转运增加。长达6小时的暴露在24小时时是可逆的。与等量的rIL-1β暴露相比，rIL-1α引起的[14C]BSA通量增加显著（P<0.01）。未发现牛和人rIL-1β之间有重要差异。跨内皮通量增加不能归因于内皮细胞毒性或生长抑制。rIL-1α与重组人肿瘤坏死因子-α之间没有相加或协同关系。我们的研究表明，IL-1α和IL-1β可能在肺血管渗漏的发病机制中起作用。
