Abstract
Clostridium perfringens enterotoxin (CPE) is responsible for causing the gastrointestinal symptoms of several C. perfringens food- and nonfood-borne human gastrointestinal diseases. The enterotoxin gene (cpe) is located on either the chromosome (for most C. perfringens type A food poisoning strains) or large conjugative plasmids (for the remaining type A food poisoning and most, if not all, other CPE-producing strains). In all CPE-positive strains, the cpe gene is strongly associated with insertion sequences that may help to assist its mobilization and spread. During disease, CPE is produced when C. perfringens sporulates in the intestines, a process involving several sporulation-specific alternative sigma factors. The action of CPE starts with its binding to claudin receptors to form a small complex; those small complexes then oligomerize to create a hexameric prepore on the membrane surface. Beta hairpin loops from the CPE molecules in the prepore assemble into a beta barrel that inserts into the membrane to form an active pore that enhances calcium influx, causing cell death. This cell death results in intestinal damage that causes fluid and electrolyte loss. CPE is now being explored for translational applications including cancer therapy/diagnosis, drug delivery, and vaccination.
Highlights
Clostridium perfringens is a preeminent pathogen of humans and livestock, causing both histotoxic diseases and illnesses originating in the intestines, namely enteritis or enterotoxemia [1]
Cloning of the cpe gene in 1993 [19] revealed that the C. perfringens enterotoxin (CPE) protein produced by a type A food poisoning strain is a single polypeptide containing 319 amino acids with a unique primary sequence
A few type E strains produce a variant CPE with 10 amino acid differences from the classical CPE made by types A, C, and D strains [6]
Summary
Clostridium perfringens is a preeminent pathogen of humans and livestock, causing both histotoxic diseases and illnesses originating in the intestines, namely enteritis or enterotoxemia (where toxins produced in the intestine are absorbed into the circulation and damage organs such as the brain) [1]. Reducing diarrhea would cause prolonged contact between the intestines and toxins like CPE, which may have facilitated the absorption of CPE into the circulation so it could damage non-intestinal organs In addition to C. perfringens type A food poisoning, CPE-positive type A strains cause several non-food-borne human gastrointestinal diseases, including about 5%–10% of all cases of antibiotic-associated diarrhea [16]. Whether CPE, when produced, contributes to type D disease is still unknown
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