Department of Biomedical Sciences and Pathobiology, VMRCVM, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA.
Inflammopharmacology. 1997;5(4):363-81. doi: 10.1007/s10787-997-0033-6.
The objective of this study was to elucidate colonic mucosal ultrastructural effects of trinitrobenzene-sulphonic acid (TNBS) with and without co-administration of recombinant human interleukin-11 (rhIL-11). Using a standard colitis model (ir alcoholic TNBS), rats were sacrificed at 3~14 days after TNBS. Co-administration of rhIL-11 (100, 300 or 1000 mug/kg sc) was given for protection, and controls received saline or alcohol ir, or rhIL-11 sc alone. Transmission electron microscopy revealed that early TNBS-induced cytopathology was primarily in absorptive cells, changes which occurred prior to goblet cell damage. Progressive cellular changes included vacuolization and increased multivesicular bodies in cell apices, disconfiguration of microvilli, enlarged Golgi apparatuses, enlargement of basal inter-cellular spaces, and eventual desquamation of epithelium and apical bursting.Organelle damage preceded surface changes and resembled ultrastructural changes reported for human ulcerative colitis. The principal effect of rhIL-11 was apparent massive release of mucus from goblet cells, filling the colonic crypts, and suggesting a mode of its protection.
本研究旨在阐明三硝基苯磺酸（TNBS）联合和不联合重组人白细胞介素-11（rhIL-11）对结肠黏膜超微结构的影响。采用标准结肠炎模型（ir 酒精 TNBS），在 TNBS 后 3~14 天处死大鼠。rhIL-11（100、300 或 1000μg/kg sc）联合给药进行保护，对照组给予生理盐水或酒精 ir，或 rhIL-11 sc 单独给药。透射电子显微镜显示，早期 TNBS 诱导的细胞病变主要发生在吸收细胞中，这些变化发生在杯状细胞损伤之前。进行性细胞变化包括细胞顶端的空泡化和多泡体增加、微绒毛排列紊乱、高尔基复合体增大、基底细胞间隙增大，最终上皮细胞脱落和顶端破裂。细胞器损伤先于表面变化，类似于人类溃疡性结肠炎的超微结构变化。rhIL-11 的主要作用是明显从杯状细胞大量释放粘液，充满结肠隐窝，提示其保护模式。
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