Log in

Relevant bibliographies by topics / Alpha toxin / Journal articles

To see the other types of publications on this topic, follow the link: Alpha toxin.

Journal articles on the topic 'Alpha toxin'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Alpha toxin.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Liang, Xudong, Meiying Yan, and Yinduo Ji. "The H35A Mutated Alpha-Toxin Interferes with Cytotoxicity of Staphylococcal Alpha-Toxin." Infection and Immunity 77, no. 3 (December 22, 2008): 977–83. http://dx.doi.org/10.1128/iai.00920-08.

Full text

Abstract:

ABSTRACT Staphylococcal alpha-toxin is an important virulence factor for Staphylococcus aureus to cause severe infections. In this study, we explored whether the toxoid of alpha-toxin may be utilized to block the toxicity of wild-type alpha-toxin. We created a series of H35A mutated alpha-toxin expression strains and revealed that the H35A mutation eliminates the activity of alpha-toxin using a human lung epithelial cell line (A549). More importantly, we found that either the pretreatment or simultaneous treatment of the epithelial cells with alpha-toxin-H35A completely disrupted the cytotoxic

APA, Harvard, Vancouver, ISO, and other styles

2

Bernheimer, Alan W. "STAPHYLOCOCCAL ALPHA TOXIN*." Annals of the New York Academy of Sciences 128, no. 1 (December 16, 2006): 112–23. http://dx.doi.org/10.1111/j.1749-6632.1965.tb11633.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Palmer. "Staphyloccal alpha toxin." Journal of Applied Microbiology 84, S1 (July 1998): 125S—126S. http://dx.doi.org/10.1046/j.1365-2672.1998.0840s1125s.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Jepson, Marie, Angela Howells, Helen L. Bullifent, Barbara Bolgiano, Dennis Crane, Julie Miller, Jane Holley, Pramukh Jayasekera, and Richard W. Titball. "Differences in the Carboxy-Terminal (Putative Phospholipid Binding) Domains of Clostridium perfringens andClostridium bifermentans Phospholipases C Influence the Hemolytic and Lethal Properties of These Enzymes." Infection and Immunity 67, no. 7 (July 1, 1999): 3297–301. http://dx.doi.org/10.1128/iai.67.7.3297-3301.1999.

Full text

Abstract:

ABSTRACT The phospholipases C of C. perfringens (alpha-toxin) and C. bifermentans (Cbp) show >50% amino acid homology but differ in their hemolytic and toxic properties. We report here the purification and characterisation of alpha-toxin and Cbp. The phospholipase C activity of alpha-toxin and Cbp was similar when tested with phosphatidylcholine in egg yolk or in liposomes. However, the hemolytic activity of alpha-toxin was more than 100-fold that of Cbp. To investigate whether differences in the carboxy-terminal domains of these proteins were responsible for differences in the hemolytic an

APA, Harvard, Vancouver, ISO, and other styles

5

Zhu, H., and H. Bussey. "Mutational analysis of the functional domains of yeast K1 killer toxin." Molecular and Cellular Biology 11, no. 1 (January 1991): 175–81. http://dx.doi.org/10.1128/mcb.11.1.175.

Full text

Abstract:

To determine the functional domains of K1 killer toxin, we analyzed the phenotypes of a set of mutations throughout regions encoding the alpha- and beta-toxin subunits that allow secretion of mutant toxins. A range of techniques have been used to examine the ability of mutant toxins to bind to beta-glucan cell wall receptor and to form lethal ion channels. Our results indicate that both the alpha and beta subunits are involved in beta-glucan receptor binding. Defects in ion channel formation and toxin immunity are confined to the hydrophobic alpha subunit of the toxin.

APA, Harvard, Vancouver, ISO, and other styles

6

Zhu, H., and H. Bussey. "Mutational analysis of the functional domains of yeast K1 killer toxin." Molecular and Cellular Biology 11, no. 1 (January 1991): 175–81. http://dx.doi.org/10.1128/mcb.11.1.175-181.1991.

Full text

Abstract:

To determine the functional domains of K1 killer toxin, we analyzed the phenotypes of a set of mutations throughout regions encoding the alpha- and beta-toxin subunits that allow secretion of mutant toxins. A range of techniques have been used to examine the ability of mutant toxins to bind to beta-glucan cell wall receptor and to form lethal ion channels. Our results indicate that both the alpha and beta subunits are involved in beta-glucan receptor binding. Defects in ion channel formation and toxin immunity are confined to the hydrophobic alpha subunit of the toxin.

APA, Harvard, Vancouver, ISO, and other styles

7

Yarovinsky, Timur O., Martha M. Monick, Matthias Husmann, and Gary W. Hunninghake. "Interferons Increase Cell Resistance to Staphylococcal Alpha-Toxin." Infection and Immunity 76, no. 2 (December 10, 2007): 571–77. http://dx.doi.org/10.1128/iai.01088-07.

Full text

Abstract:

ABSTRACT Many bacterial pathogens, including Staphylococcus aureus, use a variety of pore-forming toxins as important virulence factors. Staphylococcal alpha-toxin, a prototype β-barrel pore-forming toxin, triggers the release of proinflammatory mediators and induces primarily necrotic death in susceptible cells. However, whether host factors released in response to staphylococcal infections may increase cell resistance to alpha-toxin is not known. Here we show that prior exposure to interferons (IFNs) prevents alpha-toxin-induced membrane permeabilization, the depletion of ATP, and cell death

APA, Harvard, Vancouver, ISO, and other styles

8

TSIOURIS (Β.Σ. ΤΣΙΟΥΡΗΣ), V. S., I. GEORGOPOULOU (ΓΕΩΡΓΟΠΟΥΛΟΥ), and E. PETRIDOU (Ε. ΠΕΤΡΙΔΟΥ). "Update on the toxins of Clostridium perfringens and their actions." Journal of the Hellenic Veterinary Medical Society 61, no. 3 (November 17, 2017): 241. http://dx.doi.org/10.12681/jhvms.14892.

Full text

Abstract:

Clostridia appeared as a distinct class, approximately 2.7 billion years ago, before the initial formation of oxygen. Clostridium perfringens is widely distributed throughout the environment due to its ability to form spores. Furthermore, it is a member of intestinal microbiota in animals and human. In 2002, the complete genome of C perfringens strain 13 was published. Genomic analysis has revealed that C. perfringens lacks the genetic machinery to produce 13 essential amino acids and it obtains these in vivo via the action of its toxins. Toxins of C perfringens can be divided into major, mino

APA, Harvard, Vancouver, ISO, and other styles

9

Nilsson, Ing-Marie, Orla Hartford, Timothy Foster, and Andrzej Tarkowski. "Alpha-Toxin and Gamma-Toxin Jointly PromoteStaphylococcus aureus Virulence in Murine Septic Arthritis." Infection and Immunity 67, no. 3 (March 1, 1999): 1045–49. http://dx.doi.org/10.1128/iai.67.3.1045-1049.1999.

Full text

Abstract:

ABSTRACT Septic arthritis is a common and feared complication of staphylococcal infections. Staphylococcus aureus produces a number of potential virulence factors including certain adhesins and enterotoxins. In this study we have assessed the roles of cytolytic toxins in the development of septic arthritis by inoculating mice withS. aureus wild-type strain 8325-4 or isogenic mutants differing in the expression of alpha-, beta-, and gamma-toxin production patterns. Mice inoculated with either an alpha- or beta-toxin mutant showed degrees of inflammation, joint damage, and weight decrease simila

APA, Harvard, Vancouver, ISO, and other styles

10

Awad, Milena M., Darren M. Ellemor, Richard L. Boyd, John J. Emmins, and Julian I. Rood. "Synergistic Effects of Alpha-Toxin and Perfringolysin O in Clostridium perfringens-Mediated Gas Gangrene." Infection and Immunity 69, no. 12 (December 1, 2001): 7904–10. http://dx.doi.org/10.1128/iai.69.12.7904-7910.2001.

Full text

Abstract:

ABSTRACT To examine the synergistic effects of alpha-toxin and perfringolysin O in clostridial myonecrosis, homologous recombination was used to construct an alpha-toxin deficient derivative of a perfringolysin O mutant of Clostridium perfringens. The subsequent strain was complemented with separate plasmids that carried the alpha-toxin structural gene (plc), the perfringolysin O gene (pfoA), or both toxin genes, and the resultant isogenic strains were examined in a mouse myonecrosis model. Synergistic effects were clearly observed in these experiments. Infection with the control strain, which

APA, Harvard, Vancouver, ISO, and other styles

11

Bhakdi, S., and J. Tranum-Jensen. "Alpha-toxin of Staphylococcus aureus." Microbiological Reviews 55, no. 4 (1991): 733–51. http://dx.doi.org/10.1128/mmbr.55.4.733-751.1991.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Bhakdi, S., and J. Tranum-Jensen. "Alpha-toxin of Staphylococcus aureus." Microbiological Reviews 55, no. 4 (1991): 733–51. http://dx.doi.org/10.1128/mr.55.4.733-751.1991.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Thelestam, Monica, and Lennart Blomqvist. "Staphylococcal alpha toxin — recent advances." Toxicon 26, no. 1 (January 1988): 51–65. http://dx.doi.org/10.1016/0041-0101(88)90137-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Fisher, Derek J., Mariano E. Fernandez-Miyakawa, Sameera Sayeed, Rachael Poon, Victoria Adams, Julian I. Rood, Francisco A. Uzal, and Bruce A. McClane. "Dissecting the Contributions of Clostridium perfringens Type C Toxins to Lethality in the Mouse Intravenous Injection Model." Infection and Immunity 74, no. 9 (September 2006): 5200–5210. http://dx.doi.org/10.1128/iai.00534-06.

Full text

Abstract:

ABSTRACT The gram-positive anaerobe Clostridium perfringens produces a large arsenal of toxins that are responsible for histotoxic and enteric infections, including enterotoxemias, in humans and domestic animals. C. perfringens type C isolates, which cause rapidly fatal diseases in domestic animals and enteritis necroticans in humans, contain the genes for alpha toxin (plc), perfringolysin O (pfoA), beta toxin (cpb), and sometimes beta2 toxin (cpb2) and/or enterotoxin (cpe). Due to the economic impact of type C-induced diseases, domestic animals are commonly vaccinated with crude type C toxoid

APA, Harvard, Vancouver, ISO, and other styles

15

Tegmark, Karin, Eva Morfeldt, and Staffan Arvidson. "Regulation of agr-Dependent Virulence Genes in Staphylococcus aureus by RNAIII from Coagulase-Negative Staphylococci." Journal of Bacteriology 180, no. 12 (June 15, 1998): 3181–86. http://dx.doi.org/10.1128/jb.180.12.3181-3186.1998.

Full text

Abstract:

ABSTRACT Many of the genes coding for extracellular toxins, enzymes, and cell surface proteins in Staphylococcus aureus are regulated by a 510-nucleotide (nt) RNA molecule, RNAIII. Transcription of genes encoding secreted toxins and enzymes, includinghla (alpha-toxin), saeB (enterotoxin B),tst (toxic shock syndrome toxin 1), and ssp(serine protease), is stimulated, while transcription of genes encoding cell surface proteins, like spa (protein A) andfnb (fibronectin binding proteins), is repressed. Besides being a regulator, RNAIII is also an mRNA coding for staphylococcal delta-lysin. We have

APA, Harvard, Vancouver, ISO, and other styles

16

Sharma-Kuinkel, Batu K., Yuling Wu, David E. Tabor, Hoyin Mok, Bret R. Sellman, Amy Jenkins, Li Yu, et al. "Characterization of Alpha-ToxinhlaGene Variants, Alpha-Toxin Expression Levels, and Levels of Antibody to Alpha-Toxin in Hemodialysis and Postsurgical Patients with Staphylococcus aureus Bacteremia." Journal of Clinical Microbiology 53, no. 1 (November 12, 2014): 227–36. http://dx.doi.org/10.1128/jcm.02023-14.

Full text

Abstract:

Alpha-toxin is a majorStaphylococcus aureusvirulence factor. This study evaluated potential relationships betweenin vitroalpha-toxin expression ofS. aureusbloodstream isolates, anti-alpha-toxin antibody in serum of patients withS. aureusbacteremia (SAB), and clinical outcomes in 100 hemodialysis and 100 postsurgical SAB patients. Isolates underwentspatyping andhlasequencing. Serum anti-alpha-toxin IgG and neutralizing antibody levels were measured by using an enzyme-linked immunosorbent assay and a red blood cell (RBC)-based hemolysis neutralization assay. Neutralization of alpha-toxin by an a

APA, Harvard, Vancouver, ISO, and other styles

17

Strichartz, G. R., and G. K. Wang. "Rapid voltage-dependent dissociation of scorpion alpha-toxins coupled to Na channel inactivation in amphibian myelinated nerves." Journal of General Physiology 88, no. 3 (September 1, 1986): 413–35. http://dx.doi.org/10.1085/jgp.88.3.413.

Full text

Abstract:

The voltage-dependent action of several scorpion alpha-toxins on Na channels was studied in toad myelinated nerve under voltage clamp. These toxins slow the declining phase of macroscopic Na current, apparently by inhibiting an irreversible channel inactivation step and thus permitting channels to reopen from a closed state in depolarized membranes. In this article, we describe the rapid reversal of alpha-toxin action by membrane depolarizations more positive than +20 mV, an effect not achieved by extensive washing. Depolarizations that were increasingly positive and of longer duration caused

APA, Harvard, Vancouver, ISO, and other styles

18

Nagahama, Masahiro. "Vaccines against Clostridium perfringens Alpha-toxin." Current Pharmaceutical Biotechnology 14, no. 10 (January 31, 2014): 913–17. http://dx.doi.org/10.2174/1389201014666131226124348.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Hildebrandt, Jan‐Peter, Sabine Ziesemer, and Nils Möller. "Das alpha‐Toxin von Staphylococcus aureus." Biologie in unserer Zeit 49, no. 4 (August 2019): 270–76. http://dx.doi.org/10.1002/biuz.201910681.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

SAKURAI, Jun, Masahiro NAGAHAMA, and Sadayuki OCHI. "Action of Clostridium perfringens alpha toxin." Nippon Saikingaku Zasshi 49, no. 5/6 (1994): 719–36. http://dx.doi.org/10.3412/jsb.49.719.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Matsuda, Asami, Meiji Soe Aung, Noriko Urushibara, Mitsuyo Kawaguchiya, Ayako Sumi, Mayumi Nakamura, Yuka Horino, Masahiko Ito, Satoshi Habadera, and Nobumichi Kobayashi. "Prevalence and Genetic Diversity of Toxin Genes in Clinical Isolates of Clostridium perfringens: Coexistence of Alpha-Toxin Variant and Binary Enterotoxin Genes (bec/cpile)." Toxins 11, no. 6 (June 6, 2019): 326. http://dx.doi.org/10.3390/toxins11060326.

Full text

Abstract:

Clostridium perfringens (C. perfringens) is responsible for food-borne gastroenteritis and other infectious diseases, and toxins produced by this bacterium play a key role in pathogenesis. Although various toxins have been described for C. perfringens isolates from humans and animals, prevalence of individual toxins among clinical isolates has not yet been well explored. In the present study, a total of 798 C. perfringens clinical isolates were investigated for prevalence of eight toxin genes and their genetic diversity by PCR, nucleotide sequencing, and phylogenetic analysis. Besides the alph

APA, Harvard, Vancouver, ISO, and other styles

22

Levistre, R., M. Berguerand, G. Bereziat, and J. Masliah. "The cross-regulation of Gi-protein by cholera toxin involves a phosphorylation by protein kinase A." Biochemical Journal 306, no. 3 (March 15, 1995): 765–69. http://dx.doi.org/10.1042/bj3060765.

Full text

Abstract:

Pretreatment of alveolar macrophages with cholera toxin inhibits the release of arachidonic acid induced by the chemotactic peptide N-formylmethionyl-leucyl-phenylalanine. The results presented here show that cholera toxin might exert its inhibitory effect through the phosphorylation of Gi alpha by protein kinase A (PKA). (1) Gi-proteins from cells pretreated with cholera toxin showed parallel increases in their sensitivity to ADP-ribosylation by toxins in vitro and in Gi alpha phosphorylation. By contrast, the Gi alpha concentration was unchanged. (2) Cholera toxin pretreatment also decreased

APA, Harvard, Vancouver, ISO, and other styles

23

Leung, D. Y., M. Gately, A. Trumble, B. Ferguson-Darnell, P. M. Schlievert, and L. J. Picker. "Bacterial superantigens induce T cell expression of the skin-selective homing receptor, the cutaneous lymphocyte-associated antigen, via stimulation of interleukin 12 production." Journal of Experimental Medicine 181, no. 2 (February 1, 1995): 747–53. http://dx.doi.org/10.1084/jem.181.2.747.

Full text

Abstract:

T lymphocyte infiltration is a prominent feature of the skin inflammation associated with infections by toxin (superantigen)-secreting Staphylococcus aureus or Streptococcus bacteria. The cutaneous lymphocyte-associated antigen (CLA) has been hypothesized to be a homing receptor (HR) involved in selective migration of memory/effector T cells to the skin. Since the expression of this putative skin-selective HR is known to be under strict microenvironmental control, we sought to determine the effect of staphylococcal and streptococcal toxins on T cell expression of CLA. After in vitro stimulatio

APA, Harvard, Vancouver, ISO, and other styles

24

Niebuhr, Margarete, Merle Gathmann, Helena Scharonow, Diana Mamerow, Susanne Mommert, Hari Balaji, and Thomas Werfel. "Staphylococcal Alpha-Toxin Is a Strong Inducer of Interleukin-17 in Humans." Infection and Immunity 79, no. 4 (January 18, 2011): 1615–22. http://dx.doi.org/10.1128/iai.00958-10.

Full text

Abstract:

ABSTRACTPatients with atopic dermatitis (AD) are frequently colonized withStaphylococcus aureus, with one-third of isolates producing alpha-toxin. Moreover,S. aureuscolonization is positively correlated with the severity of eczema. Interleukin-17A (IL-17A) has gained attention in diseases associated with chronic skin infections. The aim of this study was to investigate the effects of sublytic alpha-toxin concentrations on IL-17A production. Sublytic alpha-toxin concentrations strongly induced IL-17A in peripheral blood mononuclear cells (PBMCs), isolated CD4+T cells, polarized Th17 cells, and

APA, Harvard, Vancouver, ISO, and other styles

25

Eisenhauer, Patricia B., Prasoon Chaturvedi, Richard E. Fine, Andrew J. Ritchie, Jordan S. Pober, Thomas G. Cleary, and David S. Newburg. "Tumor Necrosis Factor Alpha Increases Human Cerebral Endothelial Cell Gb3 and Sensitivity to Shiga Toxin." Infection and Immunity 69, no. 3 (March 1, 2001): 1889–94. http://dx.doi.org/10.1128/iai.69.3.1889-1894.2001.

Full text

Abstract:

ABSTRACT Hemolytic uremic syndrome (HUS) is associated with intestinal infection by enterohemorrhagic Escherichia coli strains that produce Shiga toxins. Globotriaosylceramide (Gb3) is the functional receptor for Shiga toxin, and tumor necrosis factor alpha (TNF-α) upregulates Gb3 in both human macrovascular umbilical vein endothelial cells and human microvascular brain endothelial cells. TNF-α treatment enhanced Shiga toxin binding and sensitivity to toxin. This upregulation was specific for Gb3 species containing normal fatty acids (NFA). Central nervous system (CNS) pathology in HUS could i

APA, Harvard, Vancouver, ISO, and other styles

26

McNamara, Peter J., Kathy C. Milligan-Monroe, Shirin Khalili, and Richard A. Proctor. "Identification, Cloning, and Initial Characterization of rot, a Locus Encoding a Regulator of Virulence Factor Expression in Staphylococcus aureus." Journal of Bacteriology 182, no. 11 (June 1, 2000): 3197–203. http://dx.doi.org/10.1128/jb.182.11.3197-3203.2000.

Full text

Abstract:

ABSTRACT A chromosomal insertion of transposon Tn917 partially restores the expression of protease and alpha-toxin activities to PM466, a genetically defined agr-null derivative of the wild-type Staphylococcus aureus strain RN6390. In co-transduction experiments, transposon-encoded erythromycin resistance and a protease- and alpha-toxin-positive phenotype are transferred at high frequency from mutant strains to agr-null strains ofS. aureus. Southern analysis of chromosomal DNA and sequence analysis of DNA flanking the Tn917 insertion site in mutant strains revealed that the transposon interrup

APA, Harvard, Vancouver, ISO, and other styles

27

Rodriguez, Fausto J., Matthew J. Ritter, Craig D. Tauscher, and S. Breanndan Moore. "Massive hemolysis secondary to alpha-toxin release." Transfusion 45, no. 2 (February 2005): 127. http://dx.doi.org/10.1111/j.1537-2995.2004.04206.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Schoepe, Heike, Christian Pache, Axel Neubauer, Heidrun Potschka, Tobias Schlapp, Lothar H. Wieler, and Georg Baljer. "Naturally Occurring Clostridium perfringens Nontoxic Alpha-Toxin Variant as a Potential Vaccine Candidate against Alpha-Toxin-Associated Diseases." Infection and Immunity 69, no. 11 (November 1, 2001): 7194–96. http://dx.doi.org/10.1128/iai.69.11.7194-7196.2001.

Full text

Abstract:

ABSTRACT Clostridium perfringens mutant strain 121A/91 shows neither enzymatic (phospholipase C) nor hemolytic activity. Nevertheless, the cpa gene and the corresponding alpha-toxin variant are detectable. Vaccination with this genetically constructed alpha-toxin variant, rAT121/91, induces antibodies capable of significantly reducing activities induced by wild-type toxin. Thus, rAT121/91 could be a useful vaccine candidate.

APA, Harvard, Vancouver, ISO, and other styles

29

Coursodon, Christine F., Hien T. Trinh, Michael Mallozzi, Gayatri Vedantam, R. D. Glock, and J. G. Songer. "Clostridium perfringens alpha toxin is produced in the intestines of broiler chicks inoculated with an alpha toxin mutant." Anaerobe 16, no. 6 (December 2010): 614–17. http://dx.doi.org/10.1016/j.anaerobe.2010.09.006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Ballard, J., A. Bryant, D. Stevens, and R. K. Tweten. "Purification and characterization of the lethal toxin (alpha-toxin) of Clostridium septicum." Infection and Immunity 60, no. 3 (1992): 784–90. http://dx.doi.org/10.1128/iai.60.3.784-790.1992.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Tan, Choo, Kae Tan, Tzu Ng, Si Sim, and Nget Tan. "Venom Proteome of Spine-Bellied Sea Snake (Hydrophis curtus) from Penang, Malaysia: Toxicity Correlation, Immunoprofiling and Cross-Neutralization by Sea Snake Antivenom." Toxins 11, no. 1 (December 23, 2018): 3. http://dx.doi.org/10.3390/toxins11010003.

Full text

Abstract:

The venom proteome of Hydrophis curtus (synonym: Lapemis hardwickii) from Penang, Malaysia was investigated with nano-electrospray ionization-liquid chromatography tandem mass spectrometry (ESI-LCMS/MS) of the reverse-phase high-performance liquid chromatography (HPLC) venom fractions. Thirty distinct protein forms were identified as toxins from ten families. The three major protein families were phospholipase A2 (PLA2, 62.0% of total venom proteins), three-finger toxin (3FTX, 26.33%) and cysteine-rich secretory protein (CRiSP, 9.00%). PLA2 comprises diverse homologues (11 forms), predominantl

APA, Harvard, Vancouver, ISO, and other styles

32

Kennedy, Catherine L., Dena Lyras, Leanne M. Cordner, Jody Melton-Witt, John J. Emmins, Rodney K. Tweten, and Julian I. Rood. "Pore-Forming Activity of Alpha-Toxin Is Essential for Clostridium septicum-Mediated Myonecrosis." Infection and Immunity 77, no. 3 (January 12, 2009): 943–51. http://dx.doi.org/10.1128/iai.01267-08.

Full text

Abstract:

ABSTRACT Clostridium septicum alpha-toxin is a β-barrel pore-forming cytolysin that is functionally similar to aerolysin. Residues important in receptor binding, oligomerization, and pore formation have been identified; however, little is known about the activity of the toxin in an infection, although it is essential for disease. We have now shown that deletion of a small portion of the transmembrane domain, so that the toxin is no longer able to form pores, completely abrogates its ability to contribute to disease, as does replacement of the sole cysteine residue with leucine. However, althou

APA, Harvard, Vancouver, ISO, and other styles

33

Giese, Bernd, Silvia Dittmann, Kerstin Paprotka, Katja Levin, Annett Weltrowski, Diana Biehler, Thiên-Trí Lâm, Bhanu Sinha, and Martin J. Fraunholz. "Staphylococcal Alpha-Toxin Is Not Sufficient To Mediate Escape from Phagolysosomes in Upper-Airway Epithelial Cells." Infection and Immunity 77, no. 9 (June 29, 2009): 3611–25. http://dx.doi.org/10.1128/iai.01478-08.

Full text

Abstract:

ABSTRACT Intracellular Staphylococcus aureus has been implicated in the establishment of chronic infections. It is therefore imperative to understand by what means S. aureus is able to survive within cells. Here we use two expression systems with a fluorescent readout to assay alpha-toxin expression and function within phagolysosomes of infected upper-airway epithelial cells: avirulent Staphylococcus carnosus TM300 and phenotypically alpha-toxin-negative S. aureus laboratory strains. Data from CFU recovery assays suggest that the presence of alpha-toxin is not beneficial for the intracellular

APA, Harvard, Vancouver, ISO, and other styles

34

Ellemor, Darren M., Rebecca N. Baird, Milena M. Awad, Richard L. Boyd, Julian I. Rood, and John J. Emmins. "Use of Genetically Manipulated Strains of Clostridium perfringens Reveals that Both Alpha-Toxin and Theta-Toxin Are Required for Vascular Leukostasis To Occur in Experimental Gas Gangrene." Infection and Immunity 67, no. 9 (September 1, 1999): 4902–7. http://dx.doi.org/10.1128/iai.67.9.4902-4907.1999.

Full text

Abstract:

ABSTRACT A hallmark of gas gangrene (clostridial myonecrosis) pathology is a paucity of leukocytes infiltrating the necrotic tissue. The cause of this paucity most likely relates to the observation of leukocyte aggregates at the border of the area of tissue necrosis, often within the microvasculature itself. Infecting mice with genetically manipulated strains of Clostridium perfringens type A (deficient in either alpha-toxin or theta-toxin production) resulted in significantly reduced leukocyte aggregation when alpha-toxin was absent and complete abrogation of leukocyte aggregation when theta-

APA, Harvard, Vancouver, ISO, and other styles

35

Eakes, A. T., T. K. Hymer, M. J. Rosenthal, J. Moss, and M. S. Katz. "Alterations of adenylyl cyclase-linked G proteins in rat liver during aging." American Journal of Physiology-Endocrinology and Metabolism 270, no. 1 (January 1, 1996): E126—E132. http://dx.doi.org/10.1152/ajpendo.1996.270.1.e126.

Full text

Abstract:

beta-Adrenergic stimulation of adenylyl cyclase in rat liver increases during aging. We examined whether this increase is related to alterations in the stimulatory and inhibitory G proteins (Gs and Gi) linked to adenylyl cyclase. Levels of immunoreactive alpha- and beta-subunits of Ga and Gi in liver plasma membranes from 6-, 12-, 18-, and 24-mo-old rats were unchanged with age, as was pertussis toxin-catalyzed [32P]ADP ribosylation of Gi alpha. Cholera toxin-catalyzed [32P]ADP ribosylation of Ga alpha and Gs bioactivity, assessed as reconstitution of adenylyl cyclase activity in S49 cyc- cell

APA, Harvard, Vancouver, ISO, and other styles

36

Schepers, T. M., and K. R. McLeish. "Differential cholera-toxin- and pertussis-toxin-catalysed ADP-ribosylation of G-proteins coupled to formyl-peptide and leukotriene B4 receptors." Biochemical Journal 289, no. 2 (January 15, 1993): 469–73. http://dx.doi.org/10.1042/bj2890469.

Full text

Abstract:

N-Formylmethionyl-leucyl-phenylalanine (fMet-Leu-Phe) and leukotriene B4 (LTB4) induce disparate second-messenger generation and functional responses in neutrophils and HL-60 granulocytes. Receptors for these chemoattractants couple to a common pool of G-proteins which are substrates for both pertussis-toxin- and cholera-toxin-catalysed ADP-ribosylation. The hypothesis that formyl-peptide and LTB4 receptors induce different receptor-specific conformations of activated G-proteins was tested. The ability of pertussis toxin and cholera toxin to ADP-ribosylate G(i) proteins coupled to formyl-pepti

APA, Harvard, Vancouver, ISO, and other styles

37

Panina-Bordignon, P., X. T. Fu, A. Lanzavecchia, and R. W. Karr. "Identification of HLA-DR alpha chain residues critical for binding of the toxic shock syndrome toxin superantigen." Journal of Experimental Medicine 176, no. 6 (December 1, 1992): 1779–84. http://dx.doi.org/10.1084/jem.176.6.1779.

Full text

Abstract:

Staphylococcal toxic shock syndrome toxin 1 (TSST-1) binds to major histocompatibility complex class II molecules, and the toxin-class II complexes induce proliferation of T cells expressing V beta 2 sequences. To define the residues involved in TSST-1 binding, a set of transfectants expressing 21 HLA-DR alpha chain mutants were analyzed for their abilities to bind and present TSST-1 and to present an antigenic peptide. Mutations at DR alpha positions 36 and 39 markedly decreased the ability of the DR7 molecule to bind and present TSST-1 but did not affect the ability to present an antigenic p

APA, Harvard, Vancouver, ISO, and other styles

38

Tait, A. Sasha, Monique Dalton, Blandine Geny, Felice D'Agnillo, Michel R. Popoff, and Esther M. Sternberg. "The Large Clostridial Toxins from Clostridium sordellii and C. difficile Repress Glucocorticoid Receptor Activity." Infection and Immunity 75, no. 8 (May 21, 2007): 3935–40. http://dx.doi.org/10.1128/iai.00291-07.

Full text

Abstract:

ABSTRACT We have previously shown that Bacillus anthracis lethal toxin represses glucocorticoid receptor (GR) transactivation. We now report that repression of GR activity also occurs with the large clostridial toxins produced by Clostridium sordellii and C. difficile. This was demonstrated using a transient transfection assay system for GR transactivation. We also report that C. sordellii lethal toxin inhibited GR function in an ex vivo assay, where toxin reduced the dexamethasone suppression of the proinflammatory cytokine tumor necrosis factor alpha (TNF-α). Furthermore, the glucocorticoid

APA, Harvard, Vancouver, ISO, and other styles

39

Salvarani, F. M., Z. I. P. Lobato, R. A. Assis, C. G. R. D. Lima, R. O. S. Silva, P. S. Pires, and F. C. F. Lobato. "In vitro evaluation of Clostridium septicum alpha toxoid." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 62, no. 4 (August 2010): 778–83. http://dx.doi.org/10.1590/s0102-09352010000400002.

Full text

Abstract:

Aiming to investigate in vitro alternatives, a test for neutralizing antibody detection using cell culture was developed. This test was more sensitive than previous animal models, allowing for detection of substantially lower alpha toxin and anti-alpha toxin titers. Titers observed during in vivo and in vitro seroneutralization had a correlation of 99.12%, indicating that cell culture is a viable alternative in the evaluation of vaccine potency, screening of vaccinal seeds, and Clostridium septicum alpha toxin titration.

APA, Harvard, Vancouver, ISO, and other styles

40

Braunstein, N. S., D. A. Weber, X. C. Wang, E. O. Long, and D. Karp. "Sequences in both class II major histocompatibility complex alpha and beta chains contribute to the binding of the superantigen toxic shock syndrome toxin 1." Journal of Experimental Medicine 175, no. 5 (May 1, 1992): 1301–5. http://dx.doi.org/10.1084/jem.175.5.1301.

Full text

Abstract:

Class II major histocompatibility complex (MHC) molecules present peptides derived from processed antigen to antigen-specific CD4-positive T cells. In addition, class II molecules bind with high affinity another class of antigens, termed superantigens. T cell stimulation by superantigens depends almost exclusively on the V beta segment expressed by the T cell receptor (TCR). Mapping of the superantigen binding site on class II molecules should provide valuable information on how MHC and TCR molecules interact. Recombinant mouse I-A class II molecules expressed on transfected L cells were analy

APA, Harvard, Vancouver, ISO, and other styles

41

Vázquez-Iglesias, Lorena, Borja Estefanell-Ucha, Leticia Barcia-Castro, María Páez de la Cadena, Paula Álvarez-Chaver, Daniel Ayude-Vázquez, and Francisco Javier Rodríguez-Berrocal. "A simple electroelution method for rapid protein purification: isolation and antibody production of alpha toxin fromClostridium septicum." PeerJ 5 (June 22, 2017): e3407. http://dx.doi.org/10.7717/peerj.3407.

Full text

Abstract:

Clostridium septicumproduces a number of diseases in human and farm animals which, in most of the cases, are fatal without clinical intervention. Alpha toxin is an important agent and the unique lethal virulent factor produced byClostridium septicum.This toxin is haemolytic, highly lethal and necrotizing activities but is being used as an antigen to develop animal vaccines. The aim of this study was to isolate the alpha toxin ofClostridium septicumand produce highly specific antibodies against it. In this work, we have developed a simple and efficient method for alpha toxin purification, based

APA, Harvard, Vancouver, ISO, and other styles

42

Arana, Angela M., Michael A. Bierdeman, Charles L. Balzli, Aihua Tang, Armando R. Caballero, Rupesh Patel, and Richard J. O'Callaghan. "Staphylococcus Alpha-Toxin Action on the Rabbit Iris: Toxic Effects and Their Inhibition." Current Eye Research 40, no. 8 (September 30, 2014): 830–38. http://dx.doi.org/10.3109/02713683.2014.959609.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Keyburn, Anthony L, Scott A. Sheedy, Mark E. Ford, Mark M. Williamson, Milena M. Awad, Julian I. Rood, and Robert J. Moore. "Alpha-Toxin of Clostridium perfringens Is Not an Essential Virulence Factor in Necrotic Enteritis in Chickens." Infection and Immunity 74, no. 11 (August 21, 2006): 6496–500. http://dx.doi.org/10.1128/iai.00806-06.

Full text

Abstract:

ABSTRACT The Clostridium perfringens alpha-toxin has previously been implicated as the major virulence factor in necrotic enteritis in chickens, although definitive proof has not been reported. In this study an alpha-toxin mutant was constructed in a virulent chicken isolate and shown to retain full virulence in a chicken disease model. These results demonstrated that alpha-toxin is not an essential virulence factor in the pathogenesis of necrotic enteritis in chickens.

APA, Harvard, Vancouver, ISO, and other styles

44

O'Callaghan, R. J., M. C. Callegan, J. M. Moreau, L. C. Green, T. J. Foster, O. M. Hartford, L. S. Engel, and J. M. Hill. "Specific roles of alpha-toxin and beta-toxin during Staphylococcus aureus corneal infection." Infection and immunity 65, no. 5 (1997): 1571–78. http://dx.doi.org/10.1128/iai.65.5.1571-1578.1997.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Blomqvist, L., L. E. Appelgren, and M. Thelestam. "Distribution of 3H-labeled staphylococcal alpha-toxin and a toxin fragment in mice." Infection and Immunity 55, no. 8 (1987): 1906–13. http://dx.doi.org/10.1128/iai.55.8.1906-1913.1987.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Suttorp, N., W. Seeger, E. Dewein, S. Bhakdi, and L. Roka. "Staphylococcal alpha-toxin-induced PGI2 production in endothelial cells: role of calcium." American Journal of Physiology-Cell Physiology 248, no. 1 (January 1, 1985): C127—C134. http://dx.doi.org/10.1152/ajpcell.1985.248.1.c127.

Full text

Abstract:

Studies in erythrocytes indicate that staphylococcal alpha-toxin generates discrete transmembrane channels with an effective diameter of 2-3 nm. In cultured, confluent, pig pulmonary arterial endothelial cells we studied the triggering of the arachidonic acid cascade and its dependence on calcium influx, possibly through toxin-created pores. In endothelial cells alpha-toxin time dependently (5-30 min) and dose dependently (0.1-8 micrograms/ml) stimulated the release of radiolabeled arachidonic acid and prostacyclin (PGI2) production in similar amounts as the calcium ionophore A23187 (10 microM

APA, Harvard, Vancouver, ISO, and other styles

47

Li, Jihong, Jianming Chen, Jorge E. Vidal, and Bruce A. McClane. "The Agr-Like Quorum-Sensing System Regulates Sporulation and Production of Enterotoxin and Beta2 Toxin by Clostridium perfringens Type A Non-Food-Borne Human Gastrointestinal Disease Strain F5603." Infection and Immunity 79, no. 6 (April 4, 2011): 2451–59. http://dx.doi.org/10.1128/iai.00169-11.

Full text

Abstract:

ABSTRACTClostridium perfringenstype A strains producing enterotoxin (CPE) cause one of the most common bacterial food-borne illnesses, as well as many cases of non-food-borne human gastrointestinal disease. Recent studies have shown that an Agr-like quorum-sensing system controls production of chromosomally encoded alpha-toxin and perfringolysin O byC. perfringens, as well as sporulation byClostridium botulinumandClostridium sporogenes. The current study explored whether the Agr-like quorum-sensing system also regulates sporulation and production of two plasmid-encoded toxins (CPE and beta2 to

APA, Harvard, Vancouver, ISO, and other styles

48

Maurer, Katie, Tamara Reyes-Robles, Francis Alonzo, Joan Durbin, Victor J. Torres, and Ken Cadwell. "Autophagy Mediates Tolerance to Staphylococcus aureus Alpha-Toxin." Cell Host & Microbe 17, no. 4 (April 2015): 429–40. http://dx.doi.org/10.1016/j.chom.2015.03.001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Sato, Hiroko, Joe Chiba, and Yuji Sato. "Monoclonal antibodies against alpha toxin of Clostridium perfringens." FEMS Microbiology Letters 59, no. 1-2 (May 1989): 173–76. http://dx.doi.org/10.1111/j.1574-6968.1989.tb03104.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Oda, Masataka, Yutaka Terao, Jun Sakurai, and Masahiro Nagahama. "Membrane-Binding Mechanism of Clostridium perfringens Alpha-Toxin." Toxins 7, no. 12 (December 3, 2015): 5268–75. http://dx.doi.org/10.3390/toxins7124880.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!