Cook H T, Avey C, Taylor G M
Department of Histopathology, St. Mary's Hospital Medical School, Imperial College of Science, Technology and Medicine, London, UK.
Int J Exp Pathol. 1994 Jun;75(3):157-63.
To investigate the role of interleukin-1 beta (IL-1 beta) in glomerulonephritis we studied the presence of IL-1 beta by in-situ hybridization in in-situ immune complex glomerulonephritis in the rat. Glomerulonephritis was induced in preimmunized rats by unilateral renal perfusion with cationized human IgG. In-situ hybridization was performed on frozen sections with a battery of four 30mer oligonucleotide DNA probes 3' end labelled with 35S-dATP. IL-1 beta mRNA was detectable in nephritic glomeruli at 6 and 24 hours after induction of glomerulonephritis. Signal was maximal at 48 hours and markedly reduced by 4 days. The peak of IL-1 beta transcription coincided with the major monocyte influx into glomeruli consistent with a role for IL-1 beta as a mediator of glomerular hypercellularity.
为研究白细胞介素-1β(IL-1β)在肾小球肾炎中的作用,我们通过原位杂交技术,在大鼠原位免疫复合物性肾小球肾炎模型中检测IL-1β的存在情况。采用阳离子化人IgG对预先免疫的大鼠进行单侧肾脏灌注,诱导肾小球肾炎。使用一组四个3′端用35S-dATP标记的30聚体寡核苷酸DNA探针,对冰冻切片进行原位杂交。在肾小球肾炎诱导后6小时和24小时,在肾炎性肾小球中可检测到IL-1β mRNA。信号在48小时达到峰值,4天时明显减弱。IL-1β转录的峰值与单核细胞大量流入肾小球的时间一致,这表明IL-1β作为肾小球细胞增多的介质发挥作用。