Clostridium perfringens enterotoxin

Shrestha, Archana; McClane, Bruce A.

doi:10.1016/b978-0-12-800188-2.00028-8

Cited by 3 publications

(3 citation statements)

References 101 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Also notable is the in vivo observation that, while CPE binds primarily to the villus tips in the small intestine, this toxin destroys the entire small intestinal villus (18,19). A possible insight into this phenomenon was provided by a recent study demonstrating that, in vitro, CPE-insensitive rat fibroblast cells are killed by supernatants from cultures of CPE-treated sensitive cells (20).…”

mentioning

confidence: 99%

Evidence that Clostridium perfringens Enterotoxin-Induced Intestinal Damage and Enterotoxemic Death in Mice Can Occur Independently of Intestinal Caspase-3 Activation

et al. 2018

Self Cite

View full text Add to dashboard Cite

enterotoxin (CPE) is responsible for the gastrointestinal symptoms of type A food poisoning and some cases of nonfoodborne gastrointestinal diseases, such as antibiotic-associated diarrhea. In the presence of certain predisposing medical conditions, this toxin can also be absorbed from the intestines to cause enterotoxemic death. CPE action involves intestinal damage, which begins at the villus tips. The cause of this CPE-induced intestinal damage is unknown, but CPE can induce caspase-3-mediated apoptosis in cultured enterocyte-like Caco-2 cells. Therefore, the current study evaluated whether CPE activates caspase-3 in the intestines and, if so, whether this effect is required for the development of intestinal tissue damage or enterotoxemic lethality. Using a mouse ligated small intestinal loop model, CPE was shown to cause intestinal caspase-3 activation in a dose- and time-dependent manner. Most of this caspase-3 activation occurred in epithelial cells shed from villus tips. However, CPE-induced caspase-3 activation occurred after the onset of tissue damage. Furthermore, inhibition of intestinal caspase-3 activity did not affect the onset of intestinal tissue damage. Similarly, inhibition of intestinal caspase-3 activity did not reduce CPE-induced enterotoxemic lethality in these mice. Collectively, these results demonstrate that caspase-3 activation occurs in the CPE-treated intestine but that this effect is not necessary for the development of CPE-induced intestinal tissue damage or enterotoxemic lethality.

show abstract

mentioning

confidence: 99%

Evidence that Clostridium perfringens Enterotoxin-Induced Intestinal Damage and Enterotoxemic Death in Mice Can Occur Independently of Intestinal Caspase-3 Activation

et al. 2018

Self Cite

View full text Add to dashboard Cite

show abstract

“…For example, S. aureus α-toxin, which interacts with various cell types including epithelial cells, as well as leucocidins, which target leukocytes, play a major role in S. aureus infections [ 72 , 73 ]. C. perfringens enterotoxin specifically recognizes the enterocytes and is responsible for C. perfringens foodborne poisoning [ 74 , 75 ], whereas C. perfringens ε-toxin, which is produced in the intestine, passes through the intestinal barrier without significant alteration of intestinal cells, transits in the blood circulation, targets kidney cells, crosses the blood–brain barrier, and interacts with neurons and oligodendrocytes leading to glutamate release and subsequent neurological symptoms of excitation [ 76 ].…”

Section: Bacterial Protein Toxins Active At the Cell Membranementioning

confidence: 99%

Overview of Bacterial Protein Toxins from Pathogenic Bacteria: Mode of Action and Insights into Evolution

Popoff

2024

Toxins

View full text Add to dashboard Cite

Bacterial protein toxins are secreted by certain bacteria and are responsible for mild to severe diseases in humans and animals. They are among the most potent molecules known, which are active at very low concentrations. Bacterial protein toxins exhibit a wide diversity based on size, structure, and mode of action. Upon recognition of a cell surface receptor (protein, glycoprotein, and glycolipid), they are active either at the cell surface (signal transduction, membrane damage by pore formation, or hydrolysis of membrane compound(s)) or intracellularly. Various bacterial protein toxins have the ability to enter cells, most often using an endocytosis mechanism, and to deliver the effector domain into the cytosol, where it interacts with an intracellular target(s). According to the nature of the intracellular target(s) and type of modification, various cellular effects are induced (cell death, homeostasis modification, cytoskeleton alteration, blockade of exocytosis, etc.). The various modes of action of bacterial protein toxins are illustrated with representative examples. Insights in toxin evolution are discussed.

show abstract

“…Also, that previous study used a noncellular model system (artificial membranes) lacking CPE receptors, making it necessary to evaluate the effects of mepacrine on CPE-induced cytotoxicity against host cells. This is important because, (i) the presence of receptors is essential for CPE-induced cytotoxicity at physiologically relevant CPE concentrations ( 28 , 29 ), (ii) in cells, these receptors remain associated with the CPE pore ( 11 ) and thus could affect the mepacrine sensitivity of CPE pores, and (iii) host cell responses to CPE are more complicated than those of artificial membranes, e.g., the presence of mepacrine could affect the ability of CPE-treated host cells to release membrane vesicles containing CPE pores ( 30 ) or to degrade CPE pores.…”

Section: Introductionmentioning

confidence: 99%

The Potential Therapeutic Agent Mepacrine Protects Caco-2 Cells against Clostridium perfringens Enterotoxin Action

Freedman

Hendricks

McClane

2017

mSphere

Self Cite

View full text Add to dashboard Cite

Clostridium perfringens enterotoxin (CPE) causes the gastrointestinal (GI) symptoms of a common bacterial food poisoning and several nonfoodborne human GI diseases. A previous study showed that, via an undetermined mechanism, the presence of mepacrine blocks CPE-induced electrophysiologic activity in artificial membranes. The current study now demonstrates that mepacrine also inhibits CPE-induced cytotoxicity in human enterocyte-like Caco-2 cells and that mepacrine does not directly inactivate CPE. Instead, this drug reduces both CPE pore formation and CPE pore activity in Caco-2 cells. These results suggest mepacrine as a therapeutic candidate for treating CPE-mediated GI diseases.

show abstract

Clostridium perfringens enterotoxin

Cited by 3 publications

References 101 publications

Evidence that Clostridium perfringens Enterotoxin-Induced Intestinal Damage and Enterotoxemic Death in Mice Can Occur Independently of Intestinal Caspase-3 Activation

Evidence that Clostridium perfringens Enterotoxin-Induced Intestinal Damage and Enterotoxemic Death in Mice Can Occur Independently of Intestinal Caspase-3 Activation

Overview of Bacterial Protein Toxins from Pathogenic Bacteria: Mode of Action and Insights into Evolution

The Potential Therapeutic Agent Mepacrine Protects Caco-2 Cells against Clostridium perfringens Enterotoxin Action

Contact Info

Product

Resources

About