Elliott Mark, Maignel Jacquie, Liu Sai Man, Favre-Guilmard Christine, Mir Imran, Farrow Paul, Hornby Fraser, Marlin Sandra, Palan Shilpa, Beard Matthew, Krupp Johannes
Ipsen Bioinnovation, 102 Park Drive, Milton Park, Abingdon, United Kingdom.
Ipsen Innovation, Les Ulis, France.
PLoS One. 2017 Oct 5;12(10):e0185628. doi: 10.1371/journal.pone.0185628. eCollection 2017.
Botulinum neurotoxins (BoNTs) are used extensively as therapeutic agents. Serotypes A and B are available as marketed products. Higher doses of BoNT/B are required to reach an efficacy similar to that of products containing BoNT/A. Advances in our understanding of BoNT/B mechanism of action have afforded the opportunity to make rational modifications to the toxin aimed at increasing its activity. Recently, a mutation in the light chain of BoNT/B (S201P) was described that increases the catalytic activity of the isolated BoNT/B light chain in biochemical assays. In this study, we have produced two full-length recombinant BoNT/B toxins in E.coli-one wild type (rBoNT/B1) and one incorporating the S201P mutation (rBoNT/B1(S201P)). We have compared the activity of these two molecules along with a native BoNT/B1 in biochemical cell-free assays and in several biological systems. In the cell-free assay, which measured light-chain activity alone, rBoNT/B1(S201P) cleaved VAMP-2 and VAMP-1 substrate with an activity 3-4-fold higher than rBoNT/B1. However, despite the enhanced catalytic activity of rBoNT/B1(S201P), there was no significant difference in potency between the two molecules in any of the in vitro cell-based assays, using either rodent spinal cord neurons or cortical neurons. Similarly in ex vivo tissue preparations rBoNT/B1(S201P) was not significantly more potent than rBoNT/B1 at inhibiting either diaphragm or detrusor (bladder) muscle activity in C57BL/6N and CD1 mice. Finally, no differences between rBoNT/B1 and rBoNT/B1(S201P) were observed in an in vivo digit abduction score (DAS) assay in C57BL/6N mice, either in efficacy or safety parameters. The lack of translation from the enhanced BoNT/B1(S201P) catalytic activity to potency in complex biological systems suggests that the catalytic step is not the rate-limiting factor for BoNT/B to reach maximum efficacy. In order to augment the efficacy of BoNT/B in humans, strategies other than enhancing light chain activity may need to be considered.
肉毒杆菌神经毒素(BoNTs)被广泛用作治疗药物。A 型和 B 型血清型作为市售产品可供使用。需要更高剂量的 BoNT/B 才能达到与含 BoNT/A 产品相似的疗效。我们对 BoNT/B 作用机制认识的进展为对该毒素进行合理修饰以提高其活性提供了机会。最近,有人描述了 BoNT/B 轻链中的一个突变(S201P),该突变在生化测定中增加了分离的 BoNT/B 轻链的催化活性。在本研究中,我们在大肠杆菌中产生了两种全长重组 BoNT/B 毒素——一种野生型(rBoNT/B1)和一种包含 S201P 突变的(rBoNT/B1(S201P))。我们在生化无细胞测定和几个生物系统中比较了这两种分子与天然 BoNT/B1 的活性。在仅测量轻链活性的无细胞测定中,rBoNT/B1(S201P) 切割 VAMP - 2 和 VAMP - 1 底物的活性比 rBoNT/B1 高 3 - 4 倍。然而,尽管 rBoNT/B1(S201P) 的催化活性增强,但在使用啮齿动物脊髓神经元或皮质神经元的任何体外细胞试验中,这两种分子的效力没有显著差异。同样,在离体组织制备中,在 C57BL/6N 和 CD1 小鼠中,rBoNT/B1(S201P) 在抑制膈肌或逼尿肌(膀胱)肌肉活动方面并不比 rBoNT/B1 更有效。最后,在 C57BL/6N 小鼠的体内数字外展评分(DAS)试验中,无论是在疗效还是安全性参数方面,都未观察到 rBoNT/B1 和 rBoNT/B1(S201P) 之间的差异。BoNT/B1(S201P) 增强的催化活性在复杂生物系统中未转化为效力,这表明催化步骤不是 BoNT/B 达到最大疗效的限速因素。为了提高 BoNT/B 在人类中的疗效,可能需要考虑增强轻链活性以外的策略。