Yoo H S, Maheswaran S K, Lin G, Townsend E L, Ames T R
Department of Veterinary PathoBiology, College of Veterinary Medicine, University of Minnesota, St. Paul 55108.
Infect Immun. 1995 Feb;63(2):381-8. doi: 10.1128/iai.63.2.381-388.1995.
Bovine tumor necrosis factor alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) cDNAs were generated by reverse transcription and then by PCR amplification from lipopolysaccharide (LPS)-stimulated alveolar macrophage RNA. The amplified cDNAs were cloned into pPow and expressed in Escherichia coli DH5 alpha. The expressed proteins were confirmed as TNF-alpha and IL-1 beta by Western blot (immunoblot) analysis and bioassays. We then used the cloned genes as probes in Northern (RNA) blots and investigated the kinetics of TNF-alpha and IL-1 beta mRNA expression in bovine alveolar macrophages stimulated with purified LPS from Pasteurella haemolytica 12296. The effect of LPS on TNF-alpha and IL-1 beta gene expression was dose dependent, and induction was observed at a concentration of 0.01 microgram/ml. Both TNF-alpha and IL-1 beta mRNA expression were detectable within 0.5 h after stimulation with 1 microgram of LPS per ml, peaked at 1 to 2 h, steadily declined up to 16 h, and were undetectable by 24 h. Secreted TNF-alpha measured by bioassay peaked at 4 h and accumulated at a lesser concentration in conditioned medium throughout the 24 h. By contrast, secreted IL-1 beta was induced at 8 h and reached a maximal concentration at 24 h after stimulation. The ability of LPS to induce TNF-alpha and IL-1 beta gene expression and secretion of bioactive proteins were suppressed by polymyxin B. Our findings support a role for LPS from P. haemolytica in the induction of inflammatory cytokines in bovine pneumonic pasteurellosis.
通过逆转录,然后从脂多糖(LPS)刺激的肺泡巨噬细胞RNA中进行PCR扩增,生成了牛肿瘤坏死因子α(TNF-α)和白细胞介素-1β(IL-1β)的cDNA。扩增的cDNA被克隆到pPow中,并在大肠杆菌DH5α中表达。通过蛋白质免疫印迹(免疫印迹)分析和生物测定法确认表达的蛋白质为TNF-α和IL-1β。然后,我们将克隆的基因用作Northern(RNA)印迹中的探针,并研究了用溶血巴斯德菌12296纯化的LPS刺激的牛肺泡巨噬细胞中TNF-α和IL-1β mRNA表达的动力学。LPS对TNF-α和IL-1β基因表达的影响呈剂量依赖性,在浓度为0.01微克/毫升时观察到诱导作用。在用每毫升1微克LPS刺激后0.5小时内即可检测到TNF-α和IL-1β mRNA的表达,在1至2小时达到峰值,直至16小时稳定下降,到24小时时无法检测到。通过生物测定法测得的分泌型TNF-α在4小时达到峰值,并在整个24小时内在条件培养基中以较低浓度积累。相比之下,分泌型IL-1β在刺激后8小时被诱导,并在24小时达到最大浓度。多粘菌素B抑制了LPS诱导TNF-α和IL-1β基因表达以及生物活性蛋白分泌的能力。我们的研究结果支持溶血巴斯德菌的LPS在牛肺炎性巴氏杆菌病中诱导炎性细胞因子的作用。