scholarly journals Intracellular pHluorin as Sensor for Easy Assessment of Bacteriocin-Induced Membrane-Damage in Listeria monocytogenes

2018 ◽  
Vol 9 ◽  
Author(s):  
Peter Crauwels ◽  
Leonie Schäfer ◽  
Dominik Weixler ◽  
Nadav S. Bar ◽  
Dzung B. Diep ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Membrane Damage ◽  
Induced Membrane

scholarly journals Regulation of divalent metal ions to the aggregation and membrane damage of human islet amyloid polypeptide oligomers

RSC Advances ◽  
2021 ◽  
Vol 11 (21) ◽  
pp. 12815-12825
Author(s):  
Yajie Wang ◽  
Feihong Meng ◽  
Tong Lu ◽  
Chunyun Wang ◽  
Fei Li
Keyword(s):  
Metal Ions ◽  
Metal Binding ◽  
Membrane Damage ◽  
Islet Amyloid Polypeptide ◽  
Divalent Metal ◽  
Human Islet ◽  
Divalent Metal Ions ◽  
Islet Amyloid ◽  
Induced Membrane ◽  
Human Islet Amyloid Polypeptide

Their is a counteraction between a decrease in the disruptive ability of metal-associated oligomer species and an increase in the quantity of oligomers promoted by the metal binding in the activity of hIAPP induced membrane damage.

Generation of Free Radicals and Enhancement of Hemin-induced Membrane Damage by a Catechol Iron Chelator in Plasmodium falciparum

2005 ◽  
Vol 5 (4) ◽  
pp. 463-471 ◽  
Author(s):  
B. Pradines . ◽  
F. Ramiandrasoa . ◽  
T. Fusai . ◽  
A. Hammadi . ◽  
M. Henry . ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Free Radicals ◽  
Membrane Damage ◽  
Iron Chelator ◽  
Induced Membrane

scholarly journals Sublethal Injury Caused to Listeria monocytogenes by Natural Plant Extracts: Case Study on Grape Seed Extract and Garlic Extract

2019 ◽  
Vol 9 (13) ◽  
pp. 2731 ◽  
Author(s):  
Davy Verheyen ◽  
Maria Baka ◽  
Jan F. M. Van Impe
Keyword(s):  
Listeria Monocytogenes ◽  
Plant Extracts ◽  
Membrane Damage ◽  
Grape Seed Extract ◽  
Grape Seed ◽  
Seed Extract ◽  
Food Preservation ◽  
Natural Plant ◽  
Novel Food ◽  
Sublethal Injury

Natural antimicrobials, such as grape seed extract (GSE) and garlic extract (GE), are often used as (a part of) novel food preservation technologies, especially due to their antilisterial effect. However, little is known on the extent of sublethal injury (SI) these extracts cause to Listeria monocytogenes, possibly leading to overestimated efficacies for such novel technologies. The influence of both extracts on the sublethal injury of L. monocytogenes strain LMG23775 was investigated, also using propidium iodide staining to investigate the nature of the injury. Minimum inhibitory concentrations were 500 mg gallic acid equivalents (GAE)/L and 7.5 μg allicin/mL for GSE and GE, respectively. These concentrations slowed down the growth of L. monocytogenes, while only causing a significant amount of SI for GSE. Pure extracts caused inactivation of the cells, with GSE being the most effective. Sublethal injury from pure GSE was mainly caused by membrane damage. In pure GE, a significant amount of SI, not caused by membrane damage, was also present, albeit less pronounced than in pure GSE. In conclusion, both extracts cause a significant amount of sublethal injury to L. monocytogenes, which is not taken into account in relevant studies investigating novel food preservation applications involving natural plant extracts.

The active role of Ca2+ ions in Aβ-mediated membrane damage

2018 ◽  
Vol 54 (29) ◽  
pp. 3629-3631 ◽  
Author(s):  
Michele F. M. Sciacca ◽  
Irene Monaco ◽  
Carmelo La Rosa ◽  
Danilo Milardi
Keyword(s):  
Calcium Ions ◽  
Membrane Damage ◽  
Active Role ◽  
Membrane Disruption ◽  
Induced Membrane ◽  
Membrane Poration

Calcium ions inhibits Aβ induced membrane poration by small-sized oligomers but significantly foster fiber-dependent membrane disruption.

scholarly journals Genes, pathways and risk prediction in Alzheimer’s disease

2019 ◽  
Author(s):  
John Hardy ◽  
Valentina Escott-Price
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Membrane Damage ◽  
Disease Process ◽  
Complete Understanding ◽  
Induced Membrane ◽  
Genome Wide ◽  
Key Factor ◽  
Risk Of Disease

Abstract The failure of recent clinical trials in Alzheimer's disease has highlighted the need for the development of a more complete understanding of the pathogenesis of the disorder and also a belief that therapies may only work if given very early in the disease process before overt symptoms occur. The rare, early onset forms of the disease are all caused by mutations which make amyloid deposition a more likely event. Here we discuss the recent data showing that, in contrast, much of the risk of late onset disease is encoded by loci involved in lipid metabolism and/or encoded by microglia. We discuss these finding and suggest that amyloid induced membrane damage may be a key factor in disease and also review the evidence that genome wide genetic analysis can substantially help in the prediction of those individuals at high risk of disease in the general population.

scholarly journals Enhancement of Heme-Induced Membrane Damage by the Anti-malarial Clotrimazole: the Role of Colloid-Osmotic Forces

2004 ◽  
Vol 27 (3) ◽  
pp. 361-365 ◽  
Author(s):  
Nguyen Tien Huy ◽  
Ryo Takano ◽  
Saburo Hara ◽  
Kaeko Kamei
Keyword(s):  
Membrane Damage ◽  
Induced Membrane

scholarly journals Compartmentalization of the Broad-Range Phospholipase C Activity to the Spreading Vacuole Is Critical for Listeria monocytogenes Virulence

2006 ◽  
Vol 75 (1) ◽  
pp. 44-51 ◽  
Author(s):  
P. S. Marie Yeung ◽  
Yoojin Na ◽  
Amanda J. Kreuder ◽  
Hélène Marquis
Keyword(s):  
Listeria Monocytogenes ◽  
Phospholipase C ◽  
Membrane Damage ◽  
Bacterial Pathogen ◽  
Host Cells ◽  
Virulence Attenuation ◽  
Infected Cells ◽  
Host Cell Membranes ◽  
Cell Spread

ABSTRACT Listeria monocytogenes is a bacterial pathogen that multiplies in the cytosol of host cells and spreads directly from cell to cell by using an actin-based mechanism of motility. The broad-range phospholipase C (PC-PLC) of L. monocytogenes contributes to bacterial escape from vacuoles formed upon cell-to-cell spread. PC-PLC is made as an inactive proenzyme whose activation requires cleavage of an N-terminal propeptide. During infection, PC-PLC is activated specifically in acidified vacuoles. To assess the importance of compartmentalizing PC-PLC activity during infection, we created a mutant that makes constitutively active PC-PLC (the plcBΔpro mutant). Results from intracellular growth and cell-to-cell spread assays showed that the plcBΔpro mutant was sensitive to gentamicin, suggesting that unregulated PC-PLC activity causes damage to host cell membranes. This was confirmed by the observation of a twofold increase in staining of live infected cells by a non-membrane-permeant DNA fluorescent dye. However, membrane damage was not sufficient to cause cell lysis and was dependent on bacterial cell-to-cell spread, suggesting that damage was localized to bacterium-containing filopodia. Using an in vivo competitive infection assay, we observed that the plcBΔpro mutant was outcompeted up to 200-fold by the wild-type strain in BALB/c mice. Virulence attenuation was greater when mice were infected orally than when they were infected intravenously, presumably because the plcBΔpro mutant was initially outcompeted in the intestines, reducing the number of mutant bacteria reaching the liver and spleen. Together, these results emphasize the importance for L. monocytogenes virulence of compartmentalizing the activity of PC-PLC during infection.

scholarly journals Equal Force Recovery in Dysferlin-Deficient and Wild-Type Muscles Following Saponin Exposure

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Piming Zhao ◽  
Li Xu ◽  
Younss Ait-Mou ◽  
Pieter P. de Tombe ◽  
Renzhi Han
Keyword(s):  
Muscular Dystrophy ◽  
Extensor Digitorum Longus ◽  
Membrane Damage ◽  
Force Production ◽  
Slow Muscle ◽  
Wild Type ◽  
Tetanic Force ◽  
Induced Membrane ◽  
Force Recovery ◽  
Better Than

Dysferlin plays an important role in repairing membrane damage elicited by laser irradiation, and dysferlin deficiency causes muscular dystrophy and associated cardiomyopathy. Proteins such as perforin, complement component C9, and bacteria-derived cytolysins, as well as the natural detergent saponin, can form large pores on the cell membrane via complexation with cholesterol. However, it is not clear whether dysferlin plays a role in repairing membrane damage induced by pore-forming reagents. In this study, we observed that dysferlin-deficient muscles recovered the tetanic force production to the same extent as their WT counterparts following a 5-min saponin exposure (50 μg/mL). Interestingly, the slow soleus muscles recovered significantly better than the fastextensor digitorum longus(EDL) muscles. Our data suggest that dysferlin is unlikely involved in repairing saponin-induced membrane damage and that the slow muscle is more efficient than the fast muscle in repairing such damage.

Cyclosporin A Inhibits UV-Radiation-Induced Membrane Damage but is Unable to Inhibit Carboxyatractyloside-Induced Permeability Transition

2009 ◽  
Vol 172 (5) ◽  
pp. 575-583 ◽  
Author(s):  
Noemí García ◽  
Cecilia Zazueta ◽  
Mohammed El-Hafidi ◽  
Natalia Pavón ◽  
Eduardo Martínez-Abundis ◽  
...  
Keyword(s):  
Cyclosporin A ◽  
Uv Radiation ◽  
Membrane Damage ◽  
Permeability Transition ◽  
Induced Membrane ◽  
Radiation Induced
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