Magic™ Mouse Anti-C. Perfringens epsilon Toxin Monoclonal antibody, Clone 4D6

Clostridium perfringens (C. perfringens), as an important zoonotic pathogen, is of great concern worldwide and can cause enterotoxaemia, necrotizing enterocolitis, gas gangrene and even sudden death in patients. The causative agent of the bacterium is its secretion of a variety of lethal toxins, of which the main pathogenic toxins are α, β, ε, and τ toxins, enterotoxins, and necrotic enteritis B-like toxins.

C. Perfringens epsilon toxin (ETX) can cause enterotoxaemia, a highly lethal disease with major implications for the farming industry. ETX is the third most potent bacterial toxin known after Clostridium botulinum toxin and Clostridium tetani toxin. ETX consists of three basic structural domains, initially in an inactive precursor form (proETX), which is converted to a fully active form by protease treatment. The activated toxin removes the carboxy-terminal peptide and forms an oligomeric complex on the target cell membrane, which subsequently forms a pore that causes the release of intramembrane contents and the movement of ions across the membrane, ultimately leading to cell death and organ damage. Caveolin-1 (CAV1) and caveolin-2 (CAV2) are essential for the formation of oligomeric complexes of ETX on the plasma membrane of sensitive cells. Madin-darby canine kidney (MDCK) cells are sensitive to ETX. ETX forms a giant pre-pore of heptameric complexes on the MDCK cell membrane, which is subsequently accompanied by the efflux of intracellular K⁺ and the inward flow of Na⁺ and CA²⁺, disrupting the balance of osmotic pressure inside and outside of the cell membrane, and ultimately leading to the swelling and lysis of MDCK cells. Tyrosine 43 on ETX was identified as a key residue for ETX binding to MDCK cells.

Figure 1. Representation of the Clostridium perfringens Epsilon toxin structure
(Source: Ferreira MR, et al. 2016)

ETX is considered to be an important cause of rapidly fatal enteritis and enterotoxaemia in animals. ETX can cause damage to the renal system, e.g. damage and accumulation of the toxin in the kidneys has been found in sheep suffering from enterotoxaemia, but the pathological mechanism of ETX in the kidneys is not clear. In humans, ETX is cytotoxic to human renal tubular epithelial cells. In addition, ETX damages the microvascular system and endothelial cells, leading to lung injury. ETX can also have an effect on the nervous system, causing brain damage and a number of neurological disorders. The researchers found that animals with ETX-induced enterotoxaemia also showed neurological damage. Some researchers have demonstrated by histological analysis that ETX can cause degenerative changes in hippocampus, striatum and hypothalamic neurons in rats and mice, and necrotic neurons and apoptotic cells were observed in axons with neurofilaments and demyelinated axons, which suggests that ETX can cause damage to neurons or glial cells.

Anti-Clostridium Perfringens epsilon Toxin
Anti-C. Perfringens ε Toxin
Anti-C. Perfringens ETX