Sun Y, Clinkenbeard K D, Cudd L A, Clarke C R, Clinkenbeard P A
Department of Anatomy, Pathology and Pharmacology, College of Veterinary Medicine, Oklahoma State University, Stillwater, Oklahoma 74078, USA.
Infect Immun. 1999 Dec;67(12):6264-9. doi: 10.1128/IAI.67.12.6264-6269.1999.
Pasteurella haemolytica, the causative agent of shipping fever pneumonia in cattle, produces a leukotoxin (LKT) which lyses ruminant leukocytes with high efficiency but is reputed to not affect leukocytes from nonruminant species. In this study, we tested the supposition that LKT binding correlates positively with susceptibility to intoxication of susceptible isolated bovine lymphocytes and lymphoma tissue culture cells (BL3 cells) and negatively with reputed nonsusceptible equine, porcine, and canine lymphocytes and human lymphoid tissue culture cells (Raji cells). Bovine lymphocytes and BL3 cells were highly susceptible to LKT intoxication, exhibiting both substantial increase in intracellular Ca(2+) concentration and marked leukolysis. Exposure of reputed LKT-nonsusceptible porcine lymphocytes and Raji cells to LKT caused a slightly increased intracellular Ca(2+) concentration but no leukolysis. No LKT effect was detected for equine and canine lymphocytes. LKT bound to lymphoid cells from all species tested. Intact 102-kDa LKT was recovered from exposed isolated lymphoid cell membranes. Pro-LKT acylation was not required for LKT binding to BL3 cells. LKT binding was rapid, with maximal binding occurring by 3 min, and was proportional to the LKT concentration in the range 0.04 to 4.0 microg/ml. For this LKT concentration range, BL3 cells bound more LKT than did porcine lymphocytes or Raji cells, suggesting that LKT binds to BL3 cells with higher affinity than to porcine lymphocytes or Raji cells. Above 4.0 microg/ml, LKT demonstrated saturable binding to BL3 cells. Neutralizing anti-LKT monoclonal antibody (MAb) MM601 diminished LKT binding to BL3 by 36% while decreasing leukolysis by 81%. In contrast, MM601 did not diminish LKT binding to Raji cells. Pretreatment of target cells with 120 microg of protease K per ml diminished LKT binding to BL3 cells by 75%, with only a 25% decrease in leukolysis. However, pretreatment with 150 microg of protease K per ml abolished the remaining 25% of LKT binding and 75% leukolysis. Therefore, P. haemolytica LKT binds rapidly to susceptible and to reputed nonsusceptible lymphoid cells. LKT binding resulting in species-specific leukolysis was characterized by high affinity, inhibition by MAb MM601, and relative resistance to protease K pretreatment of lymphoid cells. Two types of LKT binding to lymphoid cells are proposed. High-affinity binding leads to efficient leukolysis. In some lymphoid cells from reputed LKT-nonsusceptible species, low-affinity LKT binding may cause a low-efficiency increase in the intracellular Ca(2+) concentration without leading to leukolysis.
溶血巴斯德氏菌是牛运输热肺炎的病原体,它产生一种白细胞毒素(LKT),这种毒素能高效裂解反刍动物的白细胞,但据说对非反刍动物的白细胞没有影响。在本研究中,我们测试了这样一种假设,即LKT结合与易感的分离牛淋巴细胞和淋巴瘤组织培养细胞(BL3细胞)对中毒的易感性呈正相关,而与据认为不易感的马、猪和犬淋巴细胞以及人淋巴组织培养细胞(Raji细胞)呈负相关。牛淋巴细胞和BL3细胞对LKT中毒高度敏感,表现为细胞内Ca(2+)浓度大幅增加和明显的白细胞溶解。将据认为对LKT不易感的猪淋巴细胞和Raji细胞暴露于LKT会导致细胞内Ca(2+)浓度略有增加,但没有白细胞溶解。未检测到LKT对马和犬淋巴细胞有作用。LKT与所有测试物种的淋巴细胞结合。从暴露的分离淋巴细胞膜中回收了完整的102-kDa LKT。LKT与BL3细胞结合不需要前LKT酰化。LKT结合迅速,3分钟时达到最大结合,并且在0.04至4.0微克/毫升范围内与LKT浓度成正比。在此LKT浓度范围内,BL3细胞比猪淋巴细胞或Raji细胞结合更多的LKT,这表明LKT与BL3细胞的结合亲和力高于与猪淋巴细胞或Raji细胞的结合亲和力。高于4.0微克/毫升时,LKT对BL3细胞表现出饱和结合。中和抗LKT单克隆抗体(MAb)MM601使LKT与BL3细胞的结合减少36%,同时使白细胞溶解减少81%。相比之下,MM601没有减少LKT与Raji细胞的结合。用每毫升120微克蛋白酶K预处理靶细胞使LKT与BL3细胞的结合减少75%,白细胞溶解仅减少25%。然而,用每毫升150微克蛋白酶K预处理消除了剩余25%的LKT结合和75%的白细胞溶解。因此,溶血巴斯德氏菌LKT能迅速与易感和据认为不易感的淋巴细胞结合。导致物种特异性白细胞溶解的LKT结合的特征是高亲和力、被MAb MM601抑制以及对淋巴细胞蛋白酶K预处理相对抗性。提出了两种LKT与淋巴细胞结合的类型。高亲和力结合导致高效白细胞溶解。在一些来自据认为对LKT不易感物种的淋巴细胞中,低亲和力LKT结合可能导致细胞内Ca(2+)浓度低效增加而不导致白细胞溶解。