Relevant bibliographies by topics / Staphylococcal membrane damaging toxins

Academic literature on the topic 'Staphylococcal membrane damaging toxins'

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Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "Staphylococcal membrane damaging toxins"

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Popoff, Michel R. "Bacterial Toxins, Current Perspectives." Toxins 12, no. 9 (September 4, 2020): 570. http://dx.doi.org/10.3390/toxins12090570.

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Toxins are the major pathogenicity factors produced by numerous bacteria involved in severe diseases in humans and animals. Certain pathogenic bacteria synthesize only one toxin which is responsible for all the symptoms and outcome of the disease. For example, botulinum toxins (BoNTs) and tetanus toxin (TeNT) are the unique causal factors of botulism and tetanus, respectively. Other bacteria attack the host organism by a set of multiple toxins which synergistically act to promote the disease. This is the case of Clostridium and Staphylococcus strains which secrete wide ranges of toxins such as pore-forming toxins, membrane phospholipid damaging toxins, and other cytotoxins and toxins interacting with the immune system involved in gangrene lesion generation.
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Watanabe, Masashi, Toshio Tomita, and Tatsuji Yasuda. "Membrane-damaging action of staphylococcal alpha-toxin on phospholipid-cholesterol liposomes." Biochimica et Biophysica Acta (BBA) - Biomembranes 898, no. 3 (April 1987): 257–65. http://dx.doi.org/10.1016/0005-2736(87)90065-4.

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Nocadello, S., G. Minasov, L. Shuvalova, I. Dubrovska, E. Sabini, F. Bagnoli, G. Grandi, and W. F. Anderson. "Crystal structures of the components of theStaphylococcus aureusleukotoxin ED." Acta Crystallographica Section D Structural Biology 72, no. 1 (January 1, 2016): 113–20. http://dx.doi.org/10.1107/s2059798315023207.

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Staphylococcal leukotoxins are a family of β-barrel, bicomponent, pore-forming toxins with membrane-damaging functions. These bacterial exotoxins share sequence and structural homology and target several host-cell types. Leukotoxin ED (LukED) is one of these bicomponent pore-forming toxins thatStaphylococcus aureusproduces in order to suppress the ability of the host to contain the infection. The recent delineation of the important role that LukED plays inS. aureuspathogenesis and the identification of its protein receptors, combined with its presence inS. aureusmethicillin-resistant epidemic strains, establish this leukocidin as a possible target for the development of novel therapeutics. Here, the crystal structures of the water-soluble LukE and LukD components of LukED have been determined. The two structures illustrate the tertiary-structural variability with respect to the other leukotoxins while retaining the conservation of the residues involved in the interaction of the protomers in the bipartite leukotoxin in the pore complex.
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BUTT, H. L., R. H. DUNSTAN, N. R. McGREGOR, T. K. ROBERTS, M. ZERBES, and I. J. KLINEBERG. "An association of membrane-damaging toxins from coagulase-negative staphylococci and chronic orofacial muscle pain." Journal of Medical Microbiology 47, no. 7 (July 1, 1998): 577–84. http://dx.doi.org/10.1099/00222615-47-7-577.

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Escajadillo, Tamara, and Victor Nizet. "Pharmacological Targeting of Pore-Forming Toxins as Adjunctive Therapy for Invasive Bacterial Infection." Toxins 10, no. 12 (December 17, 2018): 542. http://dx.doi.org/10.3390/toxins10120542.

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For many of the most important human bacterial infections, invasive disease severity is fueled by the cell damaging and pro-inflammatory effects of secreted pore-forming toxins (PFTs). Isogenic PFT-knockout mutants, e.g., Staphylococcus aureus lacking α-toxin or Streptococcus pneumoniae deficient in pneumolysin, show attenuation in animal infection models. This knowledge has inspired multi-model investigations of strategies to neutralize PFTs or counteract their toxicity as a novel pharmacological approach to ameliorate disease pathogenesis in clinical disease. Promising examples of small molecule, antibody or nanotherapeutic drug candidates that directly bind and neutralize PFTs, block their oligomerization or membrane receptor interactions, plug establishment membrane pores, or boost host cell resiliency to withstand PFT action have emerged. The present review highlights these new concepts, with a special focus on β-PFTs produced by leading invasive human Gram-positive bacterial pathogens. Such anti-virulence therapies could be applied as an adjunctive therapy to antibiotic-sensitive and -resistant strains alike, and further could be free of deleterious effects that deplete the normal microflora.
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Iliya, Sani, Jonathan Mwangi, Ronald Maathai, Mary Muriuki, and Christopher Wainaina. "Molecular Detection of Panton Valentine Leukocidin Toxin in Clinical Isolates of Staphylococcus aureus from Kiambu County, Kenya." International Journal of Microbiology 2020 (August 27, 2020): 1–8. http://dx.doi.org/10.1155/2020/3106747.

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Panton–Valentine leukocidin gene is produced by Staphylococcus aureus, and methicillin-resistant Staphylococcus aureus isolates as a pore-forming toxin is largely responsible for skin and soft tissue illnesses. MRSA produces PVL toxins through lukS and lukF proteins causing tissue necrosis by damaging membrane of the defense cells. Presence of PVL toxin was tested from the 54 S. aureus clinical isolates obtained from Thika and Kiambu Level 5 Hospitals, in Kiambu County, Kenya, by Geno Type® MRSA assay (Hain Life Science, Nehren, Germany). DNA was isolated from freshly harvested bacterial cultures by spin column using Geno Type DNA isolation kit. The detection of PVL toxins was performed by amplification of genomic DNA and by reverse hybridization that identifies PVL genes using Geno Type MRSA kit. Out of 138 samples that were collected from patients in Kiambu County, 54 S. aureus isolates were obtained, of which 14 (25.9%; 95% CI = 11.9–38.9) samples had PVL toxins. The isolates that were obtained from the female patients had a higher PVL toxin prevalence of 35.7%, while the isolates collected from the male patients had a lower prevalence of 15.4% (P=0.09). The pediatrics department had the highest PVL gene prevalence compared to outpatient department and surgical units (P=0.08). However, the age groups of patients and the hospital attended by patients showed no significant difference in terms of PVL gene prevalence (P=0.26). Therefore, the patients' gender and hospital units were not significantly associated with PVL gene prevalence (P=0.08). This study shows that PVL positive isolates occur in the sampled hospitals in the county and female as well as children must be taken into consideration among patients with wound infections when isolating S. aureus.
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Gabriunaite, Inga, Gintaras Valincius, Albinas Žilinskas, and Aušra Valiūnienė. "Tethered Bilayer Membrane Formation on Silanized Fluorine Doped Tin Oxide Surface." Journal of The Electrochemical Society 169, no. 3 (March 1, 2022): 037515. http://dx.doi.org/10.1149/1945-7111/ac5c96.

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Silane compound was synthesized via click chemistry and a mixture of synthesis products without purification was used to form the self-assembled monolayers on metal oxide conducting films of fluorine doped tin oxide (FTO). Silanized FTO surfaces triggered rupture of multilamellar vesicles and formed electrically insulating tethered bilayer membranes (tBLMs). In contrast to well-known hybrid bilayer membranes on silane monolayers such as ones formed from octadecyltrichlorosilane, tBLMs on FTO contained water-ion reservoir between solid surface and phospholipid bilayer sheet. They demonstrated biological relevance and ability to reconstitute the pore-forming protein channels such as α-hemolysin from Staphylococcus aureus and melittin. The addition of cholesterol to tBLMs decreased the membrane-damaging effect of melittin, while the opposite was observed in the case of α-hemolysin. The tBLMs can be regenerated multiple times without losing their functionality. The described methodology (both synthesis and formation of anchor monolayer) can be extended to any oxide film surface by properly adjusting chemical composition of molecular anchor and silanization conditions. This makes the proposed biomimetic membrane system attractive for various applications including biomedical sensors for the detection of pore-forming toxins.
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Metcalf, Lee N., Neil R. McGregor, and Timothy K. Roberts. "Membrane Damaging Toxins from Coagulase-Negative Staphylococcus Are Associated with Self-Reported Temporomandibular Disorder (TMD) in Patients with Chronic Fatigue Syndrome." Journal of Chronic Fatigue Syndrome 12, no. 3 (January 2004): 25–43. http://dx.doi.org/10.1300/j092v12n03_03.

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Zainulabdeen, Shaimaa M. S., and Adian A. Dakl. ""Review Article Pathogenicity and virulence factors in Staphylococcus aureus." Muthanna Journal of Pure Science 8, no. 1 (January 13, 2021): 109–19. http://dx.doi.org/10.52113/2/08.01.2021/109-119.

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"Staphylococcus aureus is a pathogen that resides in the skin and nasal membranes and can cause a broad spectrum of hospital-acquired infections. These diseases are becoming more common, and treating them has become much more complicated. The pathogen’s capacity to secret a variety of host-damaging virulence factors contributes to its pathogenicity. S. aureus destroys and supersedes immune cells throughout infection via toxins and virulence proteins, yielding non-neutralizing infective antibodies which already impede adaptive immunity. S. aureus has different biofilm-forming mechanisms on devices, necrotic bone tissue, bone marrow, and finally within the osteocyte lacuno-canicular networks of living bone (OLCN).This review focuses on gaining a better understanding of S. aureus toxin-based pathogenesis and its effects on infectious diseases.
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Olofsson, Anders, Hans Hebert, Urban Kavéus, and Monica Thelestam. "Staphylococcus aureus α-Toxin Crystals on Lipid Layers: Effects of Trypsin Treatment." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 1 (August 12, 1990): 106–7. http://dx.doi.org/10.1017/s0424820100179282.

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α-toxin is a lethal, dermonecrotic, cytotoxic, and hemolytic protein which is secreted by most strains of Staphylococcus aureus . The biological effects are brought about by pertubation of membrane structures making them permeable to ions and small molecules. The structural basis for the mode of action is not known in detail. One hypothesis is that an oligomeric form of the toxin, observed both biochemically and by electron microscopy, circumscribe a hydrophilic pore through which transport can occur. Recent functional studies have demonstrated that oligomerization is a necessary but not a sufficient criterion for permeabilization. For example, trypsin treated α-toxin was, despite its lack of membrane damaging activity, able to form 200 kDa aggregates on mouse adrenocortical (Yl) tumor cells. In this work we have compared the structure of trypsin treated α-toxin with that of the intact toxin.α-toxin was purified from S. aureus strain wood 46 by isoelectric focussing and gel filtration. Tryptic toxin fragments (18 and 17 kD as determined by SDS-PAGE) were generated by digestion of native α-toxin (1 mg in 1.5 ml Tris buffered saline) with 30μg trypsin for 4 h at 37°C, pH 8.0. The reaction was terminated by the addition of 30μg lima beam trypsin inhibitor. Toxin specimens were applied to lipid layers pre-formed on carbon support films. Electron microscopy was performed after negative staining either with 1% Na-PTA (pH 7.0) or with a mixture of Na-PTA and glucose. Subsequent image processing of large coherent crystalline arrays produced correlation averaged projection maps. A three-dimensional model was obtained by collecting and combining data from tilted views.
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Dissertations / Theses on the topic "Staphylococcal membrane damaging toxins"

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McGregor, Neil Roland. "An investigation of the association between toxin producing staphylococcus, biochemical changes and jaw muscle pain." University of Sydney. Prosthetic Dentistry, 2000. http://hdl.handle.net/2123/369.

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Objectives: To assess the expression of the symptoms of jaw muscle pain and its association with alterations in biochemistry, other symptoms and the carriage of staphylococci. Methods: Three different study populations were assessed. The first was selected and examined by the author and consisted of 43 pain and 41 age and sex matched controls. The second was a study of CFS patients who were blinded to the author and the author subsequently examined the associations between jaw muscle symptom reporting and the standardised biochemistry measures. The third study was also blinded to the author but included an investigation of staphylococci and certain cytokine and biochemistry measures. Results: The three studies clearly establish an association between the carriage of toxicogenic coagulase negative staphylococci and the expression of jaw muscle pain in both males and females. These associations were homogeneous and were found whether the patients were selected on the basis of having jaw muscle pain or selected from within a population of patients selected on the basis of having Chronic Fatigue Syndrome. The studies associated the changes with variations in biochemistry and these were in turn associated with symptom expression within the jaw muscle pain patients. These biochemical alterations included the dysregulation of immune cell counts, cytokines, electrolyte and protein metabolism. These symptoms and biochemical changes were associated with pain severity and illness duration and staphylococcal toxin production. From the data a model was developed which shows the mechanisms involved in the development of chronic pain in the jaw muscles. Conclusions: The carriage of toxicogenic coagulase-negative staphylococci were found to be associated with the expression of jaw muscle pain and the alterations in biochemistry associated with these symptoms.
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McGregor, Neil Roland. "An investigation of the association between toxin producing staphylococcus, biochemical changes and jaw muscle pain." Thesis, The University of Sydney, 1999. http://hdl.handle.net/2123/369.

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Objectives: To assess the expression of the symptoms of jaw muscle pain and its association with alterations in biochemistry, other symptoms and the carriage of staphylococci. Methods: Three different study populations were assessed. The first was selected and examined by the author and consisted of 43 pain and 41 age and sex matched controls. The second was a study of CFS patients who were blinded to the author and the author subsequently examined the associations between jaw muscle symptom reporting and the standardised biochemistry measures. The third study was also blinded to the author but included an investigation of staphylococci and certain cytokine and biochemistry measures. Results: The three studies clearly establish an association between the carriage of toxicogenic coagulase negative staphylococci and the expression of jaw muscle pain in both males and females. These associations were homogeneous and were found whether the patients were selected on the basis of having jaw muscle pain or selected from within a population of patients selected on the basis of having Chronic Fatigue Syndrome. The studies associated the changes with variations in biochemistry and these were in turn associated with symptom expression within the jaw muscle pain patients. These biochemical alterations included the dysregulation of immune cell counts, cytokines, electrolyte and protein metabolism. These symptoms and biochemical changes were associated with pain severity and illness duration and staphylococcal toxin production. From the data a model was developed which shows the mechanisms involved in the development of chronic pain in the jaw muscles. Conclusions: The carriage of toxicogenic coagulase-negative staphylococci were found to be associated with the expression of jaw muscle pain and the alterations in biochemistry associated with these symptoms.
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Walker, John Arthur. "Studies of pneumolysin, the membrane damaging toxin of Streptococcus pneumoniae." Thesis, University of Leicester, 1988. http://hdl.handle.net/2381/35425.

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A recombinant phage that produced a polypeptide possessing the characteristics of pneumolysin, the membrane damaging toxin of the pneumococcus, was isolated from a bank of pneumococcal sequences in ?gt10. Subclones carrying the pneumolysin gene in various plasmids were haemolytic regardless of the orientation of the insert. The nucleotide sequence of a 5 kb fragment carrying the pneumolysin gene was determined. An open reading frame 1413 bp long was identified that when translated encoded a polypeptide with 471 amino acids and a molecular weight 52.8 kD. The N-terminal amino acid sequence of the predicted protein was identical to that of native pneumolysin. A single cysteine residue was present at position 428 in the amino acid sequence. Comparison of the DNA and amino acid sequences of pneumolysin with streptolysin O (SLO) revealed extensive homology in the amino acid sequence. The longest region of identity was a sequence of 12 amino acids surrounding the unique cysteine. A hybrid gene consisting of the 5' region of the pneumolysin gene and the 3' end of the SLO gene was constructed. The fusion polypeptide was made in E. coli, but possessed a very low haemolytic activity. Using the technique of oligonucleotide-mediated site-directed mutagenesis, two mutant genes were constructed in which the cysteine codon was changed to either a glycine or serine codon. Modified toxins when purified from E. coli had a specific activity of about 1-2 % that of wild type pneumolysin.
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Miles, Jr George Emmett. "On the structure and assembly of staphylococcal leukocidin: a study of the molecular architecture of beta-barrel pore-forming toxins." Texas A&M University, 2003. http://hdl.handle.net/1969.1/3952.

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Staphylococcal leukocidin pores are formed by the obligatory interaction of two distinct polypeptides, one of class F and one of class S, making them unique in the family of β-barrel pore-forming toxins (β-PFTs). By contrast, other β-PFTs form homooligomeric pores. For example, the staphylococcal α- hemolysin is a homoheptamer. Limited and controversial data exist on the assembly and molecular architecture of the leukocidin pore. In this work, biochemical and biophysical methods were used to characterize the leukocidin pore produced by the LukF (HlgB) and LukS (HlgC) components encoded by Staphylococcus aureus. I demonstrate that LukF and LukS assemble to form an SDS-stable pore on rabbit erythrocyte membranes. In addition, the pore-forming properties of recombinant leukocidin were investigated with planar lipid bilayers. Although leukocidins and staphylococcal α-hemolysin share partial sequence identity and related folds, LukF and LukS produce a pore with a unitary conductance of 2.5 nS (1 M KCl, 5 mM HEPES, pH 7.4), which is over three times greater than that of α-hemolysin measured under the same conditions. The subunit composition and stoichiometry of a leukocidin pore were determined by two independent methods, gel shift electrophoresis and sitespecific chemical modification during single channel recording. Four LukF and four LukS subunits were shown to co-assemble into an octameric transmembrane structure. The existence of an additional subunit in part explains properties of the leukocidin pore, such as its high conductance. Additionally, this is the first time that either technique has been applied successfully to assess the composition of a heteromeric membrane protein. It is also relevant to understanding the mechanism of assembly of β-PFT pores, and suggests new possibilities for engineering these proteins. In additional studies, the HlyII pore encoded by Bacillus cereus was found to form a homoheptameric transmembrane pore with properties conforming in general with those of other members of the class of β-PFTs. HlyII possesses additional properties which make it an attractive candidate for applications in biotechnology, such as an oligomer with a high thermal stability in the presence of SDS and the ability of the pore to remain open at high transmembrane potentials.
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Book chapters on the topic "Staphylococcal membrane damaging toxins"

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Gisou van der Goot, F. "Membrane-Damaging Toxins: Pore Formation." In Bacterial Protein Toxins, 189–202. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817893.ch13.

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Bhakdi, S. "Membrane-Damaging Toxins and Inflammation." In Symposium in Immunology VIII, 123–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59947-7_8.

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Oxhamre, Camilla, and Agneta Richter-Dahlfors. "Membrane-Damaging Toxins: Family of RTX Toxins." In Bacterial Protein Toxins, 203–14. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817893.ch14.

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Titball, Richard W., and Ajit K. Basak. "Membrane-damaging and cytotoxic phospholipases." In The Comprehensive Sourcebook of Bacterial Protein Toxins, 516–34. Elsevier, 2006. http://dx.doi.org/10.1016/b978-012088445-2/50032-9.

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Flores-Díaz, Marietta, Laura Monturiol-Gross, and Alberto Alape-Girón. "Membrane-damaging and cytotoxic sphingomyelinases and phospholipases." In The Comprehensive Sourcebook of Bacterial Protein Toxins, 627–76. Elsevier, 2015. http://dx.doi.org/10.1016/b978-0-12-800188-2.00022-7.

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Alouf, Joseph E. "Paradigms and classification of bacterial membrane-damaging toxins." In The Comprehensive Sourcebook of Bacterial Protein Toxins, 507–15. Elsevier, 2006. http://dx.doi.org/10.1016/b978-012088445-2/50031-7.

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