Assessment of the mode of action of polyhexamethylene biguanide against Listeria innocua by Fourier transformed infrared spectroscopy and fluorescence anisotropy analysis

2012 ◽  
Vol 58 (12) ◽  
pp. 1353-1361 ◽  
Author(s):  
Elise Chadeau ◽  
Emilie Dumas ◽  
Isabelle Adt ◽  
Pascal Degraeve ◽  
Claude Noël ◽  
...  
Keyword(s):  
Infrared Spectroscopy ◽  
Fluorescence Anisotropy ◽  
Mode Of Action ◽  
Cytoplasmic Membrane ◽  
Membrane Lipid ◽  
Listeria Innocua ◽  
Membrane Phospholipids ◽  
Fourier Transformed Infrared Spectroscopy ◽  
Polyhexamethylene Biguanide ◽  
Membrane Lipid Bilayer

Polyhexamethylene biguanide (PHMB) is a cationic biocide. The antibacterial mode of action of PHMB (at concentrations not exceeding its minimal inhibitory concentration) upon Listeria innocua LRGIA 01 was investigated by Fourier transformed infrared spectroscopy and fluorescence anisotropy analysis. Fourier transformed infrared spectra of bacteria treated with or without PHMB presented some differences in the lipids region: the CH2/CH3 (2924 cm–1/2960 cm–1) band areas ratio significantly increased in the presence of PHMB. Since this ratio generally reflects membrane phospholipids and membrane microenvironment of the cells, these results suggest that PHMB molecules interact with membrane phospholipids and, thus, affect membrane fluidity and conformation. To assess the hypothesis of PHMB interaction with L. innocua membrane phospholipids and to clarify the PHMB mode of action, we performed fluorescence anisotropy experiments. Two probes, 1,6-diphenyl-1,3,5-hexatriene (DPH) and its derivative 1-[4-(trimethyl-amino)-phenyl]-6-phenylhexa-1,3,5-triene (TMA-DPH), were used. DPH and TMA-DPH incorporate inside and at the surface of the cytoplasmic membrane, respectively. When PHMB was added, an increase of TMA-DPH fluorescence anisotropy was observed, but no changes of DPH fluorescence anisotropy occurred. These results are consistent with the hypothesis that PHMB molecules perturb L. innocua LRGIA 01 cytoplasmic membrane by interacting with the first layer of the membrane lipid bilayer.

Study of the influence of simulated microgravity on the cytoplasmic membrane lipid bilayer of plant cells

2015 ◽  
Vol 21 (3(94)) ◽  
pp. 40-47 ◽  
Author(s):  
T.L. Kordyum ◽  
◽  
O.M. Nedukha ◽  
V.P. Grakhov ◽  
A.K. Mel’nik ◽  
...  
Keyword(s):  
Lipid Bilayer ◽  
Simulated Microgravity ◽  
Cytoplasmic Membrane ◽  
Plant Cells ◽  
Membrane Lipid ◽  
Membrane Lipid Bilayer

Differences in CSF Phospholipid Concentration by Traumatic Brain Injury Outcome

2010 ◽  
Vol 11 (4) ◽  
pp. 325-331 ◽  
Author(s):  
Alice E. Pasvogel ◽  
Petra Miketova ◽  
Ida M. Moore
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
High Performance ◽  
Preliminary Evidence ◽  
Membrane Lipid ◽  
Normal Phase ◽  
Membrane Phospholipids ◽  
Median Concentration ◽  
Ultraviolet Detector ◽  
Membrane Lipid Bilayer

Traumatic brain injury (TBI) is a leading cause of morbidity and mortality. A cascade of events is initiated with TBI that leads to degradation of the membrane lipid bilayer of neurons and neuroglia. The purpose of this study was to (a) describe changes in the cerebrospinal fluid (CSF) phospholipid concentration over time for those who survived and those who died following TBI; and (b) determine whether there were differences in the CSF phospholipid concentration between those who survived and those who died following TBI. Thirty-nine CSF samples were obtained from 10 participants who sustained a TBI. Following extraction, phospholipids were separated and quantified by normal-phase high performance liquid chromatography with ultraviolet detector. For those who died, the highest median concentration was on Day 1 after TBI for lysophosphatidylcholine and on Day 4 after TBI for phosphatidylethanolamine, phosphatidylserine, phosphatidylcholine, and sphingomyelin. For those who survived, the highest median concentration was on Day 1 after TBI for phosphatidylcholine, on Day 3 after TBI for phosphatidylethanolamine and phosphatidylserine, on Day 4 after TBI for sphingomyelin, and on Day 5 after TBI for lysophosphatidylcholine. There were significant differences in the concentrations of phosphatidylethanolamine and phosphatidylserine on Days 1—2 and of phosphatidylethanolamine, phosphatidylcholine, and sphingomyelin on Days 3—4 after TBI between those who survived and died, with the highest concentrations in those who died. These findings provide preliminary evidence of greater disruption of central nervous system membrane phospholipids in participants who died after TBI.

scholarly journals PHLIP ARG-Mutant Interactions with the Membrane Lipid Bilayer

2021 ◽  
Vol 120 (3) ◽  
pp. 232a
Author(s):  
Hannah M. Visca ◽  
Oleg A. Andreev ◽  
Yana K. Reshetnyak
Keyword(s):  
Lipid Bilayer ◽  
Membrane Lipid ◽  
Membrane Lipid Bilayer

Time-Course of Changes in the Plasma–Membrane Lipid Bilayer and Cellular Ultrastructure Induced by Tumour Necrosis Factor-α in K 562 and Daudi Cells

1995 ◽  
Vol 23 (4) ◽  
pp. 254-263 ◽  
Author(s):  
M Marutaka ◽  
H Iwagaki ◽  
K Mizukawa ◽  
N Tanaka ◽  
K Orita
Keyword(s):  
Plasma Membrane ◽  
Cell Membrane ◽  
Membrane Fluidity ◽  
Time Course ◽  
Membrane Lipid ◽  
Plasma Membrane Lipid ◽  
Membrane Lipid Bilayer ◽  
Cell Membrane Fluidity ◽  
K 562 Cells ◽  
Factor Α

The time-course of changes in the plasma-membrane lipid bilayer induced by tumour necrosis factor-α (TNF) were investigated in cultured cells using spin-label electron-spin-resonance techniques. Treatment of K 562 cells, a human chronic myelocytic leukaemia cell line, in suspension culture with TNF for up to 6 h caused an initial increase in cell-membrane fluidity, which returned to the control level after 12 h of treatment. After 24 h of treatment, the cell-membrane fluidity had decreased and this decrease was maintained after 48 h of treatment. In Daudi cells, a human malignant lymphoma cell line, TNF, did not induce any changes in cell-membrane fluidity, indicating that the effect of TNF on membrane structure is cell-specific. The early and transient change in membrane fluidity in K 562 cells is probably related to signal generation, while the later, persistent change may reflect the phenotype of TNF-treated cells, in particular, changes in the plasma membrane-cytoplasmic complex. Histochemical electron microscopic studies indicated that the membrane fluidity changes induced by TNF have an ultrastructural correlate.

Chlorhexidine Effects on Membrane Lipid Domains of Human Buccal Epithelial Cells

1992 ◽  
Vol 71 (6) ◽  
pp. 1298-1303 ◽  
Author(s):  
K.L. Audus ◽  
M.R. Tavakoli-Saberi ◽  
H. Zheng ◽  
E.N. Boyce
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Membrane ◽  
Fluorescence Anisotropy ◽  
Membrane Lipid ◽  
Drug Induced ◽  
Lipid Packing ◽  
Drug Concentrations ◽  
Buccal Epithelial Cells ◽  
Pre Treatment

The effect of chlorhexidine gluconate on the adherence of Candida albicans to human buccal epithelial cells (BEC) and drug-induced alterations in BEC membrane-lipid packing order were examined. Treatment of BEC with attached yeasts with 0.1 and 0.2% chlorhexidine resulted in significant yeast detachment after 90 and 60 min, respectively. Following pre-treatment of BEC with > 0.1% chlorhexidine, yeast adherence was inhibited by > 80%. In parallel experiments, the fluorescence anisotropy of BEC labeled with fluorescent membrane probes-diphenylhexatriene (DPH) and trimethylammonium DPH-was assessed following exposure to chlorhexidine. The fluorescence anisotropy decreased with increasing concentrations of chlorhexidine, which indicated that the drug decreased epithelial-cell membrane-lipid packing order. Chlorhexidine concentrations that altered epithelial-cell membrane-lipid packing order, particularly in superficial regions, were similar to those drug concentrations required for detachment of adherent yeasts. Similar results were obtained with a second antifungal, nystatin A. While the effects of chlorhexidine on the buccal-cell membrane-lipid packing order were not reversed by multiple washings, the opposite situation occurred with nystatin A. The results suggest that chlorhexidine-induced alterations ofBEC membrane-lipid order may be involved in the antifungal actions of the drug.

Disorders of the red cell membrane

2020 ◽  
pp. 5456-5463
Author(s):  
Patrick G. Gallagher
Keyword(s):  
Cell Membrane ◽  
Clinical Features ◽  
Parvovirus B19 ◽  
Clinical Manifestations ◽  
Peripheral Blood Smear ◽  
Membrane Lipid ◽  
Red Cell ◽  
Red Cell Membrane ◽  
Membrane Lipid Bilayer ◽  
Parvovirus B19 Infection

The integrity of the red cell membrane depends on molecular interactions between proteins and the phospholipid membrane: vertical interactions stabilize the membrane lipid bilayer; horizontal interactions provide resistance against shear stress. Hereditary spherocytosis—affects 1 in 25 000 individuals of northern European descent. There is typically a dominant family history, but the condition is genetically heterogeneous: combined spectrin and ankyrin deficiency is the most common defect observed, followed by band 3 deficiency, isolated spectrin deficiency, and protein 4.2 deficiency. These affect vertical membrane interactions with loss of surface area relative to red cell volume. Clinical features—the key clinical manifestations are anaemia and signs of persistent haemolysis, with jaundice and a marked propensity to gallstones. Complications and treatment—parvovirus B19 infection of erythropoietic precursors may cause acute aplastic crises. Megaloblastic anaemia due to folate deficiency occurs in response to increased requirements during growth and pregnancy, but is preventable with supplementation. Splenectomy can alleviate the anaemia in many patients and reduces the risk of gallstones. Hereditary elliptocytosis—occurs with a frequency of 1 in 2000 to 1 in 4000 worldwide, and is more frequent in parts of Africa. The inheritance is usually dominant, with defects in red cell proteins such as α‎- and β‎-spectrin causing disturbances in horizontal interactions in the erythrocyte membrane. Clinical features, diagnosis, and treatment—most patients are asymptomatic and are typically diagnosed incidentally during testing for unrelated conditions, but about 10% experience haemolysis, anaemia, splenomegaly, and intermittent jaundice. Diagnosis is based on the presence of elliptocytes on a peripheral blood smear. Treatment is rarely required. Other conditions include hereditary pyropoikilocytosis, South-East Asian (or Melanesian) ovalocytosis, stomatocytosis, and acanthocytosis.

scholarly journals Haemophilus influenzae Rd Lacks a Stringently Conserved Fatty Acid Biosynthetic Enzyme and Thermal Control of Membrane Lipid Composition

2003 ◽  
Vol 185 (16) ◽  
pp. 4930-4937 ◽  
Author(s):  
Haihong Wang ◽  
John E. Cronan
Keyword(s):  
Fatty Acid ◽  
Haemophilus Influenzae ◽  
Growth Temperature ◽  
Acyl Carrier Protein ◽  
Thermal Control ◽  
Membrane Lipid ◽  
Membrane Phospholipids ◽  
E Coli ◽  
K 12

ABSTRACT The organization of the fatty acid synthetic genes of Haemophilus influenzae Rd is remarkably similar to that of the paradigm organism, Escherichia coli K-12, except that no homologue of the E. coli fabF gene is present. This finding is unexpected, since fabF is very widely distributed among bacteria and is thought to be the generic 3-ketoacyl-acyl carrier protein (ACP) synthase active on long-chain-length substrates. However, H. influenzae Rd contains a homologue of the E. coli fabB gene, which encodes a 3-ketoacyl-ACP synthase required for unsaturated fatty acid synthesis, and it seemed possible that the H. influenzae FabB homologue might have acquired the functions of FabF. E. coli mutants lacking fabF function are unable to regulate the compositions of membrane phospholipids in response to growth temperature. We report in vivo evidence that the enzyme encoded by the H. influenzae fabB gene has properties essentially identical to those of E. coli FabB and lacks FabF activity. Therefore, H. influenzae grows without FabF function. Moreover, as predicted from studies of the E. coli fabF mutants, H. influenzae is unable to change the fatty acid compositions of its membrane phospholipids with growth temperature. We also demonstrate that the fabB gene of Vibrio cholerae El Tor N16961 does not contain a frameshift mutation as was previously reported.

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