Clostridium perfringens Enterotoxin: Action, Genetics, and Translational Applications
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)...
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| Format: | Article |
| Language: | English |
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MDPI AG
2016-03-01
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| Series: | Toxins |
| Subjects: | |
| Online Access: | http://www.mdpi.com/2072-6651/8/3/73 |
| _version_ | 1798034322357223424 |
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| author | John C. Freedman Archana Shrestha Bruce A. McClane |
| author_facet | John C. Freedman Archana Shrestha Bruce A. McClane |
| author_sort | John C. Freedman |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-04-11T20:42:36Z |
| format | Article |
| id | doaj.art-793b6f888c234e809ec4184093a8f07d |
| institution | Directory Open Access Journal |
| issn | 2072-6651 |
| language | English |
| last_indexed | 2024-04-11T20:42:36Z |
| publishDate | 2016-03-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Toxins |
| spelling | doaj.art-793b6f888c234e809ec4184093a8f07d2022-12-22T04:04:10ZengMDPI AGToxins2072-66512016-03-01837310.3390/toxins8030073toxins8030073Clostridium perfringens Enterotoxin: Action, Genetics, and Translational ApplicationsJohn C. Freedman0Archana Shrestha1Bruce A. McClane2Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USADepartment of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USADepartment of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USAClostridium 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.http://www.mdpi.com/2072-6651/8/3/73Clostridium perfringensenterotoxinpore-forming toxinsporulationtight junctionsclaudins |
| spellingShingle | John C. Freedman Archana Shrestha Bruce A. McClane Clostridium perfringens Enterotoxin: Action, Genetics, and Translational Applications Toxins Clostridium perfringens enterotoxin pore-forming toxin sporulation tight junctions claudins |
| title | Clostridium perfringens Enterotoxin: Action, Genetics, and Translational Applications |
| title_full | Clostridium perfringens Enterotoxin: Action, Genetics, and Translational Applications |
| title_fullStr | Clostridium perfringens Enterotoxin: Action, Genetics, and Translational Applications |
| title_full_unstemmed | Clostridium perfringens Enterotoxin: Action, Genetics, and Translational Applications |
| title_short | Clostridium perfringens Enterotoxin: Action, Genetics, and Translational Applications |
| title_sort | clostridium perfringens enterotoxin action genetics and translational applications |
| topic | Clostridium perfringens enterotoxin pore-forming toxin sporulation tight junctions claudins |
| url | http://www.mdpi.com/2072-6651/8/3/73 |
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