Bacterial Toxins, Institut Pasteur, 75724 Paris, France.
Department of Biomedicine, Aarhus University, 8000 Aarhus, Denmark.
Toxins (Basel). 2022 May 24;14(6):364. doi: 10.3390/toxins14060364.
and are Gram-positive, spore-forming, and anaerobic bacteria that produce the most potent neurotoxins, botulinum toxin (BoNT) and tetanus toxin (TeNT), responsible for flaccid and spastic paralysis, respectively. The main habitat of these toxigenic bacteria is the environment (soil, sediments, cadavers, decayed plants, intestinal content of healthy carrier animals). can grow and produce BoNT in food, leading to food-borne botulism, and in some circumstances, can colonize the intestinal tract and induce infant botulism or adult intestinal toxemia botulism. More rarely, colonizes wounds, whereas tetanus is always a result of wound contamination by The synthesis of neurotoxins is strictly regulated by complex regulatory networks. The highest levels of neurotoxins are produced at the end of the exponential growth and in the early stationary growth phase. Both microorganisms, except E, share an alternative sigma factor, BotR and TetR, respectively, the genes of which are located upstream of the neurotoxin genes. These factors are essential for neurotoxin gene expression. and share also a two-component system (TCS) that negatively regulates neurotoxin synthesis, but each microorganism uses additional distinct sets of TCSs. Neurotoxin synthesis is interlocked with the general metabolism, and CodY, a master regulator of metabolism in Gram-positive bacteria, is involved in both clostridial species. The environmental and nutritional factors controlling neurotoxin synthesis are still poorly understood. The transition from amino acid to peptide metabolism seems to be an important factor. Moreover, a small non-coding RNA in , and quorum-sensing systems in and possibly in , also control toxin synthesis. However, both species use also distinct regulatory pathways; this reflects the adaptation of and to different ecological niches.
和 是革兰氏阳性、产芽孢、厌氧细菌，它们产生最有效的神经毒素，肉毒杆菌毒素（BoNT）和破伤风毒素（TeNT），分别导致弛缓和痉挛性瘫痪。这些产毒细菌的主要栖息地是环境（土壤、沉积物、尸体、腐烂植物、健康载体动物的肠道内容物）。 可以在食物中生长并产生 BoNT，导致食源性肉毒中毒，在某些情况下， 可以定植肠道并引起婴儿肉毒中毒或成人肠毒血症肉毒中毒。更罕见的是， 定植于伤口，而破伤风总是由 污染伤口引起。神经毒素的合成受到复杂调控网络的严格调控。在指数生长期末期和早期静止生长期，神经毒素的产量最高。除 E 外，这两种微生物都共享一个替代 sigma 因子，分别为 BotR 和 TetR，它们的基因位于神经毒素基因的上游。这些因子对于神经毒素基因的表达是必不可少的。 和 还共享一个负调控神经毒素合成的双组分系统（TCS），但每种微生物都使用额外的、独特的 TCS 集合。神经毒素的合成与一般代谢相联锁，而 CodY 是革兰氏阳性菌代谢的主要调节剂，参与两种梭菌的调控。控制神经毒素合成的环境和营养因素仍知之甚少。从氨基酸到肽代谢的转变似乎是一个重要因素。此外， 中的一个小非编码 RNA 和 中的群体感应系统以及可能在 中的群体感应系统也控制毒素的合成。然而，这两个物种也使用不同的调控途径；这反映了 和 对不同生态位的适应。
