Normal and Abnormal Intestinal Absorption by Humans
Shayne C. Gad in Toxicology of the Gastrointestinal Tract, 2018
Clostridium perfringens type A produces a 35 kDa enterotoxin (CPE) that is an important cause of food poisoning, human non-foodborne GI disease, and some veterinary GI diseases. CPE action involves formation of complexes in mammalian plasma membranes. One such complex of approximately 155 kDa is responsible for plasma membrane permeability alterations, which result in enterotoxin-treated mammalian cell death. Such membrane permeability changes also damage the epithelium, allowing the enterotoxin to interact with the tight junction (TJ) protein occludin. CPE:occludin interacts to form an approximately 200 kDa CPE complex and the internalization of occludin into the cytoplasm. Removal of occludin (and possibly other proteins) damages TJs and disrupts the normal paracellular permeability barrier of the intestinal epithelium, which may contribute to CPE-induced diarrhea. Low CPE doses kill mammalian cells by inducing a classic apoptotic pathway involving mitochondrial membrane depolarization, cytochrome C release, and caspase 3/7 activation. High enterotoxin doses, however, induce oncosis, which is a proinflammatory event. CPE is a unique, multifunctional toxin with cytotoxic, TJ-damaging, and potentially significant proinflammatory action [74].
Management of bacterial skin and skin structure infections with polymicrobial etiology
Published in Expert Review of Anti-infective Therapy, 2019
Silvano Esposito, Tiziana Ascione, Pasquale Pagliano
S. aureus and GABHS, alone or in synergism, are also the most common pathogens of necrotizing fasciitis. However, other aerobic and anaerobic pathogens may be present [24]. Clostridium perfringens is the most common Clostridium spp. causing the clostridial myonecrosis and C. septicum and other species (C. novyi, C. bifermentans, C. histolyticum, and C. fallax) can be the causative agents [25]. Moreover, Gram-positive cocci, especially S. aureus, are the main pathogens causing diabetic foot infections, but Gram-negative pathogens can be reported in those with chronic infection receiving multiple antibiotic treatments [26]. Infections in patients suffering foot ischemia or gangrene can be caused by obligate anaerobic pathogens [27]. In Table 2 is summarized the cause according the risk factor and the type of SSTI.
The role of claudin-4 in the development of gastric cancer
Published in Scandinavian Journal of Gastroenterology, 2020
Clostridium perfringens enterotoxin (CPE) can lead to gastrointestinal symptoms. CPE acts by binding to the claudin receptors to form complexes that create porous structures on the surface membranes of cells, thus increasing calcium influx and leading to cell death [61]. Claudin-4 is a target of CPE [62]. A Claudin-4-targeted therapy molecule (C-CPE-PSIF) is a conjugate of the C-terminal fragment of Clostridium perfringens enterotoxin with the protein synthesis inhibitory factor derived from Pseudomonas aeruginosa exotoxin. Intra-tumour injection of C-CPE-PSIF inhibited tumour growth [63]. Studies in rats revealed that claudin-4 was a safe target for GC therapy [64]. Therefore, claudin-4 can serve as a potential therapeutic target in the treatment of GC. Current studies are exploring whether claudin-4 can be applied to regulate the sensitivity of GC cells to chemotherapy in vitro, revealing promising application potential. Studies targeting the inhibitory effect of claudin-4 molecules on tumours in animals are lacking. These studies should be performed in the future.
Clostridium perfringens: a rare cause of spondylodiscitis case report and review of the literature
Published in British Journal of Neurosurgery, 2018
M. Seller, R.D. Burghardt, T. Rolling, N. Hansen-Algenstaedt, C. Schaefer
Clostridium perfringens in general are likely to be susceptible to penicillin and clindamycin.1 Penicillin G has been shown to penetrate the intervertebral disk in an in vitro model. Clindamycin reached therapeutic levels in the intervertebral discs of rabbits. According to these studies clindamycin or a combination of clindamycin and penicillin seems to be an alternative antimicrobial regimen to penicillin alone for discitis caused by Clostridium perfringens, but there are no available data of clinical efficacy. Surgical intervention seems warranted when neurological damage is present. There is no available data on spondylitis due to Clostridium perfringens, as ours is the first published case, but our combined management of surgical debridement and antimicrobial therapy with penicillin G had a favorable outcome.
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