Disease relevance of Clostridium

• One pathway, found in Desulfovibrio and Clostridium, involves reduction of TNT to triaminotoluene; subsequent steps are still not known [1].
• Cephalosporin-associated pseudomembranous colitis due to Clostridium difficile [2].
• The invasive capacity of Shigella flexneri for Chinese hamister ovary (CHO) cells and other epithelial cells were greatly reduced when treated with Clostridium botulinum exoenzyme C3 transferase [3].
• Alpha toxin from Clostridium perfringens type A, a phospholipase C, has been implicated in many of the localized and systemic features of gas gangrene [4].
• Genetic deficiency in the chemokine receptor CCR1 protects against acute Clostridium difficile toxin A enteritis in mice [5].

Psychiatry related information on Clostridium

• One hundred patients, known to have been excreting Clostridium difficile cytotoxin in faeces, were reviewed retrospectively to determine the response time for treatment with oral metronidazole and vancomycin, and the effect of the additional administration of anti-motility agents [6].

High impact information on Clostridium

• Epidemics of diarrhea caused by a clindamycin-resistant strain of Clostridium difficile in four hospitals [7].
• Perfringolysin O (PFO), a water-soluble monomeric cytolysin secreted by pathogenic Clostridium perfringens, oligomerizes and forms large pores upon encountering cholesterol-containing membranes [8].
• BACKGROUND: Large outbreaks of diarrhea caused by a newly recognized strain of Clostridium difficile occurred in four hospitals located in different parts of the United States between 1989 and 1992 [7].
• Glucosylation of Rho proteins by Clostridium difficile toxin B [9].
• Translocation of PHAKT-GFP is inhibited by toxin-B from Clostridium difficile, indicating that it requires activity of one or more Rho guanosine triphosphatases [10].

Chemical compound and disease context of Clostridium

• Vegetative cells of Clostridium botulinum were shown to contain iron-sulfur proteins that react with added nitrite to form iron-nitric oxide complexes, with resultant destruction of the iron-sulfur cluster [11].
• Disrupting Nt-Syr1 function by cleavage with Clostridium botulinum type C toxin or competition with a soluble fragment of Nt-Syr1 prevents potassium and chloride ion channel response to ABA in guard cells and implicates Nt-Syr1 in an ABA-signaling cascade [12].
• Some Clostridium species may reduce TNT to hydroxylaminodinitrotoluenes, which are then further metabolized [1].
• Rho proteins, which are involved in receptor-mediated regulation of the actin cytoskeleton, are substrates for ADP-ribosylation by Clostridium botulinum C3 toxins [13].
• Application of Clostridium difficile toxin B, an inhibitor of the Rho family of GTPases, at the Aplysia sensory to motor neuron synapse blocks long-term facilitation and the associated growth of new sensory neuron varicosities induced by repeated pulses of serotonin (5-HT) [14].

Biological context of Clostridium

• The transmission electron microscopy images provide unequivocal evidence that the fungal family 1 CBMs as well as the family 3 CBM from Clostridium thermocellum CipA have defined binding sites on two opposite corners of Valonia cellulose crystals [15].
• The substrate specificity of thermophilic xylose isomerase from Clostridium thermosulfurogenes was examined by using predictions from the known crystal structure of the Arthrobacter enzyme and site-directed mutagenesis of the thermophile xylA gene [16].
• Intrarectal instillation of azoxymethane appreciably increased the multiplicity of colonic tumors in germ-free rats and in gnotobiotic rats contaminated with Clostridium perfringens, as compared to conventional controls [17].
• The deduced amino acid sequence shows significant identity (34%) to a PSD-like sequence from Clostridium pasteurianum and the yeast PSD1 (19%) at the carboxyl end of the protein [18].
• Fluorescence resonance energy transfer was used to monitor aggregation kinetics of the "thiol-activated" cytolysin (perfringolysin O (PFO) or theta-toxin) of Clostridium perfringens on erythrocyte membranes [19].

Anatomical context of Clostridium

• Scrape loading Clostridium botulinum C3 exoenzyme into primary peripheral blood human T lymphocytes (PB T cells) efficiently adenosine diphosphate (ADP)-ribosylates and thus inactivates the guanosine triphosphatase (GTPase) Rho [20].
• Diminished Clostridium difficile toxin A sensitivity in newborn rabbit ileum is associated with decreased toxin A receptor [21].
• The intestinal effects of Clostridium difficile toxin A are inidated by toxin binding to luminal enterocyte receptors [22].
• Pectate lyase A, an enzymatic subunit of the Clostridium cellulovorans cellulosome [23].
• These actin-containing structures were also induced by injection of Clostridium botulinum C3 exoenzyme, which abolishes RhoA-mediated functions such as neurite retraction [24].

Gene context of Clostridium

• Claudin-4: a new target for pancreatic cancer treatment using Clostridium perfringens enterotoxin [25].
• Clostridium difficile toxin B activates the EGF receptor and the ERK/MAP kinase pathway in human colonocytes [26].
• Leptin mediates Clostridium difficile toxin A-induced enteritis in mice [27].
• In Saccharomyces cerevisiae the ras-related protein Rho1p is essentially the only target for ADP-ribosylation by exoenzyme C3 of Clostridium botulinum [28].
• These results are also consistent with those obtained in heterologous expression of spinach and Clostridium acidiurici monofunctional synthetases in ade3 strains [29].

Analytical, diagnostic and therapeutic context of Clostridium

• In cell culture (NIH-3T3, rat basophilic leukemia cells) toxin A inhibits Clostridium botulinum ADP-ribosyltransferase C3 (C3)-catalyzed ADP-ribosylation of the low molecular mass GTP-binding Rho proteins [30].
• Microinjection of the inhibitory exchange factor Rho-guanine nucleotide dissociation inhibitor (GDI), or Clostridium botulinum C3 ADP-ribosyl transferase (C3) toxin, a Rho-ADP-ribosylating exoenzyme, potently inhibited migration [31].
• Molecular cloning and functional characterization of the receptor for Clostridium perfringens enterotoxin [32].
• The molecular size of the phosphorylated band decreased slightly following treatment with Clostridium botulinum type A neurotoxin, whereas the band disappeared after treatment with botulinum type E neurotoxin, indicating that the 28-kDa protein was SNAP-25 [33].
• The effectiveness of a ten-day course of either oral bacitracin or oral vancomycin hydrochloride for treatment of Clostridium difficile-induced antibiotic-associated diarrhea was compared in a randomized double-blind study [34].

References