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Disease relevance of Clostridium


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


Anatomical context of Clostridium


Gene context of Clostridium


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].


  1. Biological degradation of 2,4,6-trinitrotoluene. Esteve-Núñez, A., Caballero, A., Ramos, J.L. Microbiol. Mol. Biol. Rev. (2001) [Pubmed]
  2. Cephalosporin-associated pseudomembranous colitis due to Clostridium difficile. Bartlett, J.G., Willey, S.H., Chang, T.W., Lowe, B. JAMA (1979) [Pubmed]
  3. rho, a small GTP-binding protein, is essential for Shigella invasion of epithelial cells. Watarai, M., Kamata, Y., Kozaki, S., Sasakawa, C. J. Exp. Med. (1997) [Pubmed]
  4. Alpha toxin from Clostridium perfringens induces proinflammatory changes in endothelial cells. Bunting, M., Lorant, D.E., Bryant, A.E., Zimmerman, G.A., McIntyre, T.M., Stevens, D.L., Prescott, S.M. J. Clin. Invest. (1997) [Pubmed]
  5. Genetic deficiency in the chemokine receptor CCR1 protects against acute Clostridium difficile toxin A enteritis in mice. Morteau, O., Castagliuolo, I., Mykoniatis, A., Zacks, J., Wlk, M., Lu, B., Pothoulakis, C., Gerard, N.P., Gerard, C. Gastroenterology (2002) [Pubmed]
  6. Diarrhoea caused by Clostridium difficile: response time for treatment with metronidazole and vancomycin. Wilcox, M.H., Howe, R. J. Antimicrob. Chemother. (1995) [Pubmed]
  7. Epidemics of diarrhea caused by a clindamycin-resistant strain of Clostridium difficile in four hospitals. Johnson, S., Samore, M.H., Farrow, K.A., Killgore, G.E., Tenover, F.C., Lyras, D., Rood, J.I., DeGirolami, P., Baltch, A.L., Rafferty, M.E., Pear, S.M., Gerding, D.N. N. Engl. J. Med. (1999) [Pubmed]
  8. The mechanism of membrane insertion for a cholesterol-dependent cytolysin: a novel paradigm for pore-forming toxins. Shatursky, O., Heuck, A.P., Shepard, L.A., Rossjohn, J., Parker, M.W., Johnson, A.E., Tweten, R.K. Cell (1999) [Pubmed]
  9. Glucosylation of Rho proteins by Clostridium difficile toxin B. Just, I., Selzer, J., Wilm, M., von Eichel-Streiber, C., Mann, M., Aktories, K. Nature (1995) [Pubmed]
  10. Polarization of chemoattractant receptor signaling during neutrophil chemotaxis. Servant, G., Weiner, O.D., Herzmark, P., Balla, T., Sedat, J.W., Bourne, H.R. Science (2000) [Pubmed]
  11. Nitrite inhibition of Clostridium botulinum: electron spin resonance detection of iron-nitric oxide complexes. Reddy, D., Lancaster, J.R., Cornforth, D.P. Science (1983) [Pubmed]
  12. A tobacco syntaxin with a role in hormonal control of guard cell ion channels. Leyman, B., Geelen, D., Quintero, F.J., Blatt, M.R. Science (1999) [Pubmed]
  13. Monoglucosylation of low-molecular-mass GTP-binding Rho proteins by clostridial cytotoxins. Aktories, K., Just, I. Trends Cell Biol. (1995) [Pubmed]
  14. Serotonin-induced regulation of the actin network for learning-related synaptic growth requires Cdc42, N-WASP, and PAK in Aplysia sensory neurons. Udo, H., Jin, I., Kim, J.H., Li, H.L., Youn, T., Hawkins, R.D., Kandel, E.R., Bailey, C.H. Neuron (2005) [Pubmed]
  15. The binding specificity and affinity determinants of family 1 and family 3 cellulose binding modules. Lehtiö, J., Sugiyama, J., Gustavsson, M., Fransson, L., Linder, M., Teeri, T.T. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  16. Switching substrate preference of thermophilic xylose isomerase from D-xylose to D-glucose by redesigning the substrate binding pocket. Meng, M., Lee, C., Bagdasarian, M., Zeikus, J.G. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
  17. Colon carcinogenesis with azoxymethane and dimethylhydrazine in germ-free rats. Reddy, B.S., Narisawa, T., Wright, P., Vukusich, D., Weisburger, J.H., Wynder, E.L. Cancer Res. (1975) [Pubmed]
  18. Phosphatidylserine decarboxylase 2 of Saccharomyces cerevisiáe. Cloning and mapping of the gene, heterologous expression, and creation of the null allele. Trotter, P.J., Pedretti, J., Yates, R., Voelker, D.R. J. Biol. Chem. (1995) [Pubmed]
  19. Kinetic aspects of the aggregation of Clostridium perfringens theta-toxin on erythrocyte membranes. A fluorescence energy transfer study. Harris, R.W., Sims, P.J., Tweten, R.K. J. Biol. Chem. (1991) [Pubmed]
  20. Adenosine diphosphate (ADP)-ribosylation of the guanosine triphosphatase (GTPase) rho in resting peripheral blood human T lymphocytes results in pseudopodial extension and the inhibition of T cell activation. Woodside, D.G., Wooten, D.K., McIntyre, B.W. J. Exp. Med. (1998) [Pubmed]
  21. Diminished Clostridium difficile toxin A sensitivity in newborn rabbit ileum is associated with decreased toxin A receptor. Eglow, R., Pothoulakis, C., Itzkowitz, S., Israel, E.J., O'Keane, C.J., Gong, D., Gao, N., Xu, Y.L., Walker, W.A., LaMont, J.T. J. Clin. Invest. (1992) [Pubmed]
  22. Rabbit sucrase-isomaltase contains a functional intestinal receptor for Clostridium difficile toxin A. Pothoulakis, C., Gilbert, R.J., Cladaras, C., Castagliuolo, I., Semenza, G., Hitti, Y., Montcrief, J.S., Linevsky, J., Kelly, C.P., Nikulasson, S., Desai, H.P., Wilkins, T.D., LaMont, J.T. J. Clin. Invest. (1996) [Pubmed]
  23. Pectate lyase A, an enzymatic subunit of the Clostridium cellulovorans cellulosome. Tamaru, Y., Doi, R.H. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  24. Rho family GTPases and neuronal growth cone remodelling: relationship between increased complexity induced by Cdc42Hs, Rac1, and acetylcholine and collapse induced by RhoA and lysophosphatidic acid. Kozma, R., Sarner, S., Ahmed, S., Lim, L. Mol. Cell. Biol. (1997) [Pubmed]
  25. Claudin-4: a new target for pancreatic cancer treatment using Clostridium perfringens enterotoxin. Michl, P., Buchholz, M., Rolke, M., Kunsch, S., Löhr, M., McClane, B., Tsukita, S., Leder, G., Adler, G., Gress, T.M. Gastroenterology (2001) [Pubmed]
  26. Clostridium difficile toxin B activates the EGF receptor and the ERK/MAP kinase pathway in human colonocytes. Na, X., Zhao, D., Koon, H.W., Kim, H., Husmark, J., Moyer, M.P., Pothoulakis, C., LaMont, J.T. Gastroenterology (2005) [Pubmed]
  27. Leptin mediates Clostridium difficile toxin A-induced enteritis in mice. Mykoniatis, A., Anton, P.M., Wlk, M., Wang, C.C., Ungsunan, L., Blüher, S., Venihaki, M., Simeonidis, S., Zacks, J., Zhao, D., Sougioultzis, S., Karalis, K., Mantzoros, C., Pothoulakis, C. Gastroenterology (2003) [Pubmed]
  28. The small GTP-binding protein Rho1p is localized on the Golgi apparatus and post-Golgi vesicles in Saccharomyces cerevisiae. McCaffrey, M., Johnson, J.S., Goud, B., Myers, A.M., Rossier, J., Popoff, M.R., Madaule, P., Boquet, P. J. Cell Biol. (1991) [Pubmed]
  29. Function of yeast cytoplasmic C1-tetrahydrofolate synthase. Song, J.M., Rabinowitz, J.C. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  30. The low molecular mass GTP-binding protein Rho is affected by toxin A from Clostridium difficile. Just, I., Selzer, J., von Eichel-Streiber, C., Aktories, K. J. Clin. Invest. (1995) [Pubmed]
  31. Rho proteins play a critical role in cell migration during the early phase of mucosal restitution. Santos, M.F., McCormack, S.A., Guo, Z., Okolicany, J., Zheng, Y., Johnson, L.R., Tigyi, G. J. Clin. Invest. (1997) [Pubmed]
  32. Molecular cloning and functional characterization of the receptor for Clostridium perfringens enterotoxin. Katahira, J., Inoue, N., Horiguchi, Y., Matsuda, M., Sugimoto, N. J. Cell Biol. (1997) [Pubmed]
  33. Phosphorylation of 25-kDa synaptosome-associated protein. Possible involvement in protein kinase C-mediated regulation of neurotransmitter release. Shimazaki, Y., Nishiki, T., Omori, A., Sekiguchi, M., Kamata, Y., Kozaki, S., Takahashi, M. J. Biol. Chem. (1996) [Pubmed]
  34. Oral bacitracin vs vancomycin therapy for Clostridium difficile-induced diarrhea. A randomized double-blind trial. Dudley, M.N., McLaughlin, J.C., Carrington, G., Frick, J., Nightingale, C.H., Quintiliani, R. Arch. Intern. Med. (1986) [Pubmed]
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