LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 11

Search options

  1. Book ; Online ; Thesis: Elektrophysiologische Veränderungen des Netzwerkverhaltens im MK-801 Tiermodell

    Kehrer, Colin [Verfasser]

    2010  

    Author's details Colin Kehrer
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Publisher Medizinische Fakultät Charité - Universitätsmedizin Berlin
    Publishing place Berlin
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

    More links

    Kategorien

  2. Article ; Online: Altered Excitatory-Inhibitory Balance in the NMDA-Hypofunction Model of Schizophrenia.

    Kehrer, Colin / Maziashvili, Nino / Dugladze, Tamar / Gloveli, Tengis

    Frontiers in molecular neuroscience

    2008  Volume 1, Page(s) 6

    Abstract: Schizophrenia is a common psychiatric disorder of high incidence, affecting approximately 1% of the world population. The essential neurotransmitter pathology of schizophrenia remains poorly defined, despite huge advances over the past half-century in ... ...

    Abstract Schizophrenia is a common psychiatric disorder of high incidence, affecting approximately 1% of the world population. The essential neurotransmitter pathology of schizophrenia remains poorly defined, despite huge advances over the past half-century in identifying neurochemical and pathological abnormalities in the disease. The dopamine/serotonin hypothesis has originally provided much of the momentum for neurochemical research in schizophrenia. In recent years, the attention has, however, shifted to the glutamate system, the major excitatory neurotransmitter in the CNS and towards a concept of functional imbalance between excitatory and inhibitory transmission at the network level in various brain regions in schizophrenia. The evidence indicating a central role for the NMDA-receptor subtype in the aetiology of schizophrenia has led to the NMDA-hypofunction model of this disease and the use of phencyclidines as a means to induce the NMDA-hypofunction state in animal models. The purpose of this review is to discuss recent findings highlighting the importance of the NMDA-hypofunction model of schizophrenia, both from a clinical perspective, as well as in opening a line of research, which enables electrophysiological studies at the cellular and network level in vitro. In particular, changes in excitation-inhibition (E/I) balance in the NMDA-hypofunction model of the disease and the resulting changes in network behaviours, particularly in gamma frequency oscillatory activity, will be discussed.
    Language English
    Publishing date 2008-04-08
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452967-9
    ISSN 1662-5099 ; 1662-5099
    ISSN (online) 1662-5099
    ISSN 1662-5099
    DOI 10.3389/neuro.02.006.2008
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article ; Online: Discovery and intranasal administration of a SARS-CoV-2 broadly acting neutralizing antibody with activity against multiple Omicron subvariants.

    Duty, J Andrew / Kraus, Thomas / Zhou, Heyue / Zhang, Yanliang / Shaabani, Namir / Yildiz, Soner / Du, Na / Singh, Alok / Miorin, Lisa / Li, Donghui / Stegman, Karen / Ophir, Sabrina / Cao, Xia / Atanasoff, Kristina / Lim, Reyna / Mena, Ignacio / Bouvier, Nicole M / Kowdle, Shreyas / Carreño, Juan Manuel /
    Rivero-Nava, Laura / Raskin, Ariel / Moreno, Elena / Johnson, Sachi / Rathnasinghe, Raveen / Pai, Chin I / Kehrer, Thomas / Cabral, Elizabeth Paz / Jangra, Sonia / Healy, Laura / Singh, Gagandeep / Warang, Prajakta / Simon, Viviana / Sordillo, Emilia Mia / van Bakel, Harm / Liu, Yonghong / Sun, Weina / Kerwin, Lisa / Teijaro, John / Schotsaert, Michael / Krammer, Florian / Bresson, Damien / García-Sastre, Adolfo / Fu, Yanwen / Lee, Benhur / Powers, Colin / Moran, Thomas / Ji, Henry / Tortorella, Domenico / Allen, Robert

    Med (New York, N.Y.)

    2022  Volume 3, Issue 10, Page(s) 705–721.e11

    Abstract: Background: The continual emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern, in particular the newly emerged Omicron (B.1.1.529) variant and its BA.X lineages, has rendered ineffective a number of previously ... ...

    Abstract Background: The continual emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern, in particular the newly emerged Omicron (B.1.1.529) variant and its BA.X lineages, has rendered ineffective a number of previously FDA emergency use authorized SARS-CoV-2 neutralizing antibody therapies. Furthermore, those approved antibodies with neutralizing activity against Omicron BA.1 are reportedly ineffective against the subset of Omicron subvariants that contain a R346K substitution, BA.1.1, and the more recently emergent BA.2, demonstrating the continued need for discovery and characterization of candidate therapeutic antibodies with the breadth and potency of neutralizing activity required to treat newly diagnosed COVID-19 linked to recently emerged variants of concern.
    Methods: Following a campaign of antibody discovery based on the vaccination of Harbor H2L2 mice with defined SARS-CoV-2 spike domains, we have characterized the activity of a large collection of spike-binding antibodies and identified a lead neutralizing human IgG1 LALA antibody, STI-9167.
    Findings: STI-9167 has potent, broad-spectrum neutralizing activity against the current SARS-COV-2 variants of concern and retained activity against each of the tested Omicron subvariants in both pseudotype and live virus neutralization assays. Furthermore, STI-9167 nAb administered intranasally or intravenously provided protection against weight loss and reduced virus lung titers to levels below the limit of quantitation in Omicron-infected K18-hACE2 transgenic mice.
    Conclusions: With this established activity profile, a cGMP cell line has been developed and used to produce cGMP drug product intended for intravenous or intranasal use in human clinical trials.
    Funding: Funded by CRIPT (no. 75N93021R00014), DARPA (HR0011-19-2-0020), and NCI Seronet (U54CA260560).
    MeSH term(s) Administration, Intranasal ; Animals ; Antibodies, Neutralizing/therapeutic use ; Antibodies, Viral/therapeutic use ; Humans ; Immunoglobulin G ; Membrane Glycoproteins ; Mice ; Neutralization Tests ; SARS-CoV-2/genetics ; Spike Glycoprotein, Coronavirus/genetics ; Viral Envelope Proteins ; COVID-19 Drug Treatment
    Chemical Substances Antibodies, Neutralizing ; Antibodies, Viral ; Immunoglobulin G ; Membrane Glycoproteins ; Spike Glycoprotein, Coronavirus ; Viral Envelope Proteins ; spike protein, SARS-CoV-2
    Language English
    Publishing date 2022-08-08
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ISSN 2666-6340
    ISSN (online) 2666-6340
    DOI 10.1016/j.medj.2022.08.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article ; Online: Met carriers of BDNF Val66Met genotype show increased N-acetylaspartate concentration in the anterior cingulate cortex.

    Gallinat, Jürgen / Schubert, Florian / Brühl, Rüdiger / Hellweg, Rainer / Klär, Andreas A / Kehrer, Colin / Wirth, Christoph / Sander, Thomas / Lang, Undine E

    NeuroImage

    2010  Volume 49, Issue 1, Page(s) 767–771

    Abstract: Decreased levels of N-acetylaspartate (NAA) and brain-derived neurotrophic factor (BDNF) in the anterior cingulate cortex (ACC) have been linked to neuronal loss and psychiatric disorders like schizophrenia and bipolar disorder. We previously found that ... ...

    Abstract Decreased levels of N-acetylaspartate (NAA) and brain-derived neurotrophic factor (BDNF) in the anterior cingulate cortex (ACC) have been linked to neuronal loss and psychiatric disorders like schizophrenia and bipolar disorder. We previously found that BDNF serum concentration was predicted by the concentration of NAA in the ACC, indicating that neuronal integrity and vitality of a cortical region like the ACC, as reflected by a high concentration of NAA, might be related to high concentrations of BDNF in serum. Moreover, our recent finding that Val66Met genotype appears to predict the BDNF serum level in healthy human volunteers suggests the Met allele to be connected to higher concentrations of BDNF in serum. We examined absolute NAA concentrations in the ACC and hippocampus of 40 male and 42 female healthy volunteers (age: 33.3+/-9 years). We found NAA in the ACC to be significantly increased in Met carriers (F=5.2, df=1, p=0.025). On the other hand, the concentration of creatine+phosphocreatine in the hippocampus was significantly decreased in Met carriers. We hypothesize that higher NAA levels in the ACC might contribute to the protection of Met allele carriers against major psychiatric disorders as schizophrenia and bipolar disorder.
    MeSH term(s) Adult ; Amino Acid Substitution ; Analysis of Variance ; Aspartic Acid/analogs & derivatives ; Aspartic Acid/metabolism ; Brain Chemistry/genetics ; Brain Chemistry/physiology ; Brain-Derived Neurotrophic Factor/genetics ; Cerebral Cortex/metabolism ; Choline/metabolism ; Creatine/metabolism ; Female ; Genotype ; Heterozygote ; Hippocampus/metabolism ; Humans ; Magnetic Resonance Spectroscopy ; Male ; Methionine/genetics ; Methionine/physiology ; Neurons/physiology ; Polymorphism, Single Nucleotide ; Valine/genetics ; Valine/physiology
    Chemical Substances Brain-Derived Neurotrophic Factor ; Aspartic Acid (30KYC7MIAI) ; N-acetylaspartate (997-55-7) ; Methionine (AE28F7PNPL) ; Valine (HG18B9YRS7) ; Creatine (MU72812GK0) ; Choline (N91BDP6H0X)
    Language English
    Publishing date 2010-01-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1147767-2
    ISSN 1095-9572 ; 1053-8119
    ISSN (online) 1095-9572
    ISSN 1053-8119
    DOI 10.1016/j.neuroimage.2009.08.018
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article: Increased inhibitory input to CA1 pyramidal cells alters hippocampal gamma frequency oscillations in the MK-801 model of acute psychosis.

    Kehrer, Colin / Dugladze, Tamar / Maziashvili, Nino / Wójtowicz, Anna / Schmitz, Dietmar / Heinemann, Uwe / Gloveli, Tengis

    Neurobiology of disease

    2007  Volume 25, Issue 3, Page(s) 545–552

    Abstract: The phencyclidine compound MK-801 can induce psychosis with symptoms which closely resemble those observed in an acute schizophrenic episode. Here we used an in vitro model of psychosis after systemic administration of MK-801. We found that kainate- ... ...

    Abstract The phencyclidine compound MK-801 can induce psychosis with symptoms which closely resemble those observed in an acute schizophrenic episode. Here we used an in vitro model of psychosis after systemic administration of MK-801. We found that kainate-induced gamma frequency field oscillations in animals previously exposed to MK-801 have significantly higher power than in control animals. The intrinsic membrane properties of pyramidal cells, such as membrane input resistance and time constant, were not found to be different. In contrast, the MK-801 cells exhibited significantly more depolarized resting membrane potentials than control cells. We propose cellular alterations in Na+-K+-pump activity and increases in phasic inhibition in MK-801 cells to be the respective underlying mechanisms responsible for the more depolarized resting membrane potentials and the increased power of gamma frequency oscillations observed in MK-801 pretreated animals.
    MeSH term(s) Acute Disease ; Animals ; Disease Models, Animal ; Dizocilpine Maleate/pharmacology ; Enzyme Inhibitors/pharmacology ; Excitatory Amino Acid Agonists/pharmacology ; Excitatory Amino Acid Antagonists/pharmacology ; Hippocampus/cytology ; Hippocampus/drug effects ; Hippocampus/physiopathology ; Inhibitory Postsynaptic Potentials/drug effects ; Inhibitory Postsynaptic Potentials/physiology ; Kainic Acid/pharmacology ; Mice ; Mice, Inbred C57BL ; Neural Inhibition/drug effects ; Organ Culture Techniques ; Ouabain/pharmacology ; Psychoses, Substance-Induced/physiopathology ; Pyramidal Cells/drug effects ; Pyramidal Cells/physiology ; Schizophrenia/chemically induced ; Schizophrenia/physiopathology ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors ; Sodium-Potassium-Exchanging ATPase/metabolism
    Chemical Substances Enzyme Inhibitors ; Excitatory Amino Acid Agonists ; Excitatory Amino Acid Antagonists ; Ouabain (5ACL011P69) ; Dizocilpine Maleate (6LR8C1B66Q) ; Sodium-Potassium-Exchanging ATPase (EC 3.6.3.9) ; Kainic Acid (SIV03811UC)
    Language English
    Publishing date 2007-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1211786-9
    ISSN 1095-953X ; 0969-9961
    ISSN (online) 1095-953X
    ISSN 0969-9961
    DOI 10.1016/j.nbd.2006.10.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article ; Online: Discovery of a SARS-CoV-2 Broadly-Acting Neutralizing Antibody with Activity against Omicron and Omicron + R346K Variants

    Duty, J. Andrew / Kraus, Thomas A / Zhou, Heyue / Zhang, Yanliang / Shaabani, Namir / Yildiz, Soner / Du, Na / Singh, Alok / Miorin, Lisa / Li, Donghui / Stegman, Karen / Ophir, Sabrina I / Cao, Xia / Atanasoff, Kristina / Lim, Reyna / Kowdle, Shreyas S / Carreno, Juan Manuel / Rivero-Nava, Laura / Raskin, Ariel /
    Moreno, Elena / Johnson, Sachi / Rathnasinghe, Raveen / Pai, Chin I / Kehrer, Thomas / Paz Cabral, Elizabeth / Jangra, Sonia / Healy, Laura D / Singh, Gagandeep / Warang, Prajakta / Simon, Viviana / Sordillo, Mia Emilia / van Bakel, Harm / Liu, Yonghong / Sun, Weina / Kerwin, Lisa / Palese, Peter / Teijaro, John / Schotsaert, Michael / Krammer, Florian / Bresson, Damien / Garcia-Sastre, Adolfo / Fu, Yanwen / Lee, Benhur / Powers, Colin / Moran, Thomas M / Ji, Henry / Tortorella, Domenico / Allen, Robert D

    bioRxiv

    Abstract: The continual emergence of SARS-CoV-2 variants of concern, in particular the newly emerged Omicron (B.1.1.529) variant, has rendered ineffective a number of previously EUA approved SARS-CoV-2 neutralizing antibody therapies. Furthermore, even those ... ...

    Abstract The continual emergence of SARS-CoV-2 variants of concern, in particular the newly emerged Omicron (B.1.1.529) variant, has rendered ineffective a number of previously EUA approved SARS-CoV-2 neutralizing antibody therapies. Furthermore, even those approved antibodies with neutralizing activity against Omicron are reportedly ineffective against the subset of Omicron variants that contain a R346K substitution, demonstrating the continued need for discovery and characterization of candidate therapeutic antibodies with the breadth and potency of neutralizing activity required to treat newly diagnosed COVID-19 linked to recently emerged variants of concern. Following a campaign of antibody discovery based on the vaccination of Harbour H2L2 mice with defined SARS-CoV-2 spike domains, we have characterized the activity of a large collection of Spike-binding antibodies and identified a lead neutralizing human IgG1 LALA antibody, STI-9167. STI-9167 has potent, broad-spectrum neutralizing activity against the current SARS-COV-2 variants of concern and retained activity against the Omicron and Omicron + R346K variants in both pseudotype and live virus neutralization assays. Furthermore, STI-9167 nAb administered intranasally or intravenously provided protection against weight loss and reduced virus lung titers to levels below the limit of quantitation in Omicron-infected K18-hACE2 transgenic mice. With this established activity profile, a cGMP cell line has been developed and used to produce cGMP drug product intended for use in human clinical trials.
    Keywords covid19
    Language English
    Publishing date 2022-01-20
    Publisher Cold Spring Harbor Laboratory
    Document type Article ; Online
    DOI 10.1101/2022.01.19.476998
    Database COVID19

    Kategorien

  7. Article: Effects of phencyclidines on signal transfer from the entorhinal cortex to the hippocampus in rats.

    Dugladze, Tamar / Lepsveridze, Eka / Breustedt, Jörg / Kehrer, Colin / Heinemann, Uwe / Gloveli, Tengis

    Neuroscience letters

    2003  Volume 354, Issue 3, Page(s) 185–188

    Abstract: The information transfer from the superficial layers of the entorhinal cortex (EC) to the hippocampus is regulated in a frequency dependent manner. Phencyclidine and related compounds such as MK-801 produce psychotic symptoms that closely resemble ... ...

    Abstract The information transfer from the superficial layers of the entorhinal cortex (EC) to the hippocampus is regulated in a frequency dependent manner. Phencyclidine and related compounds such as MK-801 produce psychotic symptoms that closely resemble schizophrenia. We studied the effects of systemic administration of MK-801 on the signal transfer from the EC layer III to the hippocampal area CA1. High frequency (above 10 Hz) activation of the bi-synaptic entorhinal input in control animals results in a strong suppression of the field potentials in the stratum lacunosum-moleculare of the area CA1. In contrast, in MK-801 pretreated rats the field response was less reduced. The field potential responses evoked in these two groups of animals by high-frequency activation of the monosynaptic input were similar suggesting selective alterations in layer III of the medial EC. We suggest, that MK-801 causes disinhibition of layer III projection cells and, therefore, may cause strong, pathological activation of direct layer III-CA1 pathway.
    MeSH term(s) Action Potentials/drug effects ; Animals ; Animals, Newborn ; Dizocilpine Maleate/pharmacology ; Dose-Response Relationship, Radiation ; Electric Stimulation/methods ; Entorhinal Cortex/anatomy & histology ; Entorhinal Cortex/drug effects ; Entorhinal Cortex/physiology ; Excitatory Amino Acid Antagonists/pharmacology ; Female ; Hippocampus/anatomy & histology ; Hippocampus/drug effects ; Hippocampus/physiology ; In Vitro Techniques ; Neural Conduction/drug effects ; Neural Pathways/anatomy & histology ; Neural Pathways/drug effects ; Neural Pathways/physiology ; Phencyclidine/pharmacology ; Rats
    Chemical Substances Excitatory Amino Acid Antagonists ; Dizocilpine Maleate (6LR8C1B66Q) ; Phencyclidine (J1DOI7UV76)
    Language English
    Publishing date 2003-10-17
    Publishing country Ireland
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 194929-9
    ISSN 1872-7972 ; 0304-3940
    ISSN (online) 1872-7972
    ISSN 0304-3940
    DOI 10.1016/j.neulet.2003.10.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article ; Online: Juvenile metachromatic leukodystrophy 10 years post transplant compared with a non-transplanted cohort.

    Krägeloh-Mann, I / Groeschel, S / Kehrer, C / Opherk, K / Nägele, T / Handgretinger, R / Müller, I

    Bone marrow transplantation

    2012  Volume 48, Issue 3, Page(s) 369–375

    Abstract: ... demonstrated a reversal of the initial choline increase and N-acetyl-aspartate (NAA) decrease. Only axonal ...

    Abstract Metachromatic leukodystrophy (MLD) is a rare inborn error of metabolism leading to severe neurological symptoms and early death. Hematopoietic SCT (HSCT) is considered a treatment option, but results are inconsistent and comparison with natural history is practically missing. We compare a girl with juvenile MLD 10 years after allogeneic HSCT not only with her untreated sister, but also with a large cohort of untreated patients. The girl received HSCT at the age of 5 years when first motor signs appeared. Over 10 years she was stable with respect to her clinical course and gained cognitive abilities. Magnetic resonance imaging (MRI) showed clear regression of white matter changes and magnetic resonance spectroscopy (MRS) demonstrated a reversal of the initial choline increase and N-acetyl-aspartate (NAA) decrease. Only axonal demyelinating neuropathy showed some progression. Her gross motor function and MRI-scores were clearly better compared with her sister and the cohort of untreated patients. Difference to her sister became apparent only 4 years after HSCT. We conclude that HSCT, early in the course of disease, can lead to stabilization of juvenile MLD with a course clearly different from the natural history. HSCT may prevent disease progression, if performed sufficient time before loss of walking, which typically initiates rapid deterioration.
    MeSH term(s) Adolescent ; Cohort Studies ; Disease Progression ; Female ; Hematopoietic Stem Cell Transplantation/methods ; Humans ; Leukodystrophy, Metachromatic/diagnosis ; Leukodystrophy, Metachromatic/pathology ; Leukodystrophy, Metachromatic/surgery ; Male ; Treatment Outcome
    Language English
    Publishing date 2012-09-03
    Publishing country England
    Document type Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 632854-4
    ISSN 1476-5365 ; 0268-3369 ; 0951-3078
    ISSN (online) 1476-5365
    ISSN 0268-3369 ; 0951-3078
    DOI 10.1038/bmt.2012.155
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  9. Article: Free radicals: a potential pathogenic mechanism in inherited muscular dystrophy.

    Murphy, M E / Kehrer, J P

    Life sciences

    1986  Volume 39, Issue 24, Page(s) 2271–2278

    Abstract: Despite years of intensive work, the biochemical defect responsible for the pathogenesis of inherited muscular dystrophy has not been identified either in humans or animal models. This review examines evidence in support of the hypothesis that free ... ...

    Abstract Despite years of intensive work, the biochemical defect responsible for the pathogenesis of inherited muscular dystrophy has not been identified either in humans or animal models. This review examines evidence in support of the hypothesis that free radicals may be responsible for muscle degeneration in this disorder. A variety of cellular abnormalities noted in dystrophic muscles can be accounted for by free radical mediated damage. In addition, chemical by-products associated with free radical damage are found in dystrophic muscle tissue from humans and animals with this disease. Various enzymatic antioxidant systems can be enhanced as a normal cellular response to oxidative stress, and such changes are seen both in dystrophic muscle cells and certain other tissues of dystrophic animals. An increased level of free radical damage would follow from either: enhanced production of free radical species, or a deficient component of the cellular antioxidant system, such as vitamin E. The free radical hypothesis of muscular dystrophy can account for data supporting several alternative theories of the pathogenesis of this disease, as well as other observations which have not previously been explained.
    MeSH term(s) Calcium/metabolism ; Collagen/metabolism ; Free Radicals ; Glycerylphosphorylcholine/metabolism ; Membranes/physiology ; Microcirculation ; Muscles/blood supply ; Muscles/cytology ; Muscular Dystrophies/complications ; Muscular Dystrophies/physiopathology ; Serotonin/metabolism ; Vitamin E Deficiency/complications
    Chemical Substances Free Radicals ; Serotonin (333DO1RDJY) ; Glycerylphosphorylcholine (60M22SGW66) ; Collagen (9007-34-5) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 1986-12-15
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/0024-3205(86)90657-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  10. Article: Phospholipase A secreted by Legionella pneumophila destroys alveolar surfactant phospholipids.

    Flieger, A / Gongab, S / Faigle, M / Mayer, H A / Kehrer, U / Mussotter, J / Bartmann, P / Neumeister, B

    FEMS microbiology letters

    2000  Volume 188, Issue 2, Page(s) 129–133

    Abstract: ... serogroup 6. Free fatty acids and lysophosphatidylcholine were formed, the latter is known to be highly ...

    Abstract Destruction of alveolar surfactant phospholipids by bacterial phospholipases is suggested to be a major virulence factor involved in bacterial pneumonia. Since Legionella pneumophila secretes phospholipase A, we analyzed phospholipid degradation in natural bovine surfactant by L. pneumophila. Phospholipids were reduced in amount after incubation with bacteria or culture supernatant of L. pneumophila serogroup 6. Free fatty acids and lysophosphatidylcholine were formed, the latter is known to be highly cytotoxic. Surface tension of surfactant as determined by pulsating bubble surfactometer increased significantly compared to the control. Phospholipase A activity seems to be a powerful agent of legionellae in causing lung disease.
    MeSH term(s) Animals ; Cattle ; Fatty Acids/analysis ; Legionella pneumophila/enzymology ; Legionella pneumophila/growth & development ; Lysophosphatidylcholines/analysis ; Magnetic Resonance Spectroscopy ; Phosphatidylcholines/analysis ; Phosphatidylglycerols/analysis ; Phospholipases A/metabolism ; Pulmonary Surfactants/analysis ; Pulmonary Surfactants/chemistry ; Pulmonary Surfactants/metabolism ; Surface Tension ; Time Factors
    Chemical Substances Fatty Acids ; Lysophosphatidylcholines ; Phosphatidylcholines ; Phosphatidylglycerols ; Pulmonary Surfactants ; Phospholipases A (EC 3.1.1.32)
    Language English
    Publishing date 2000-07-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 752343-9
    ISSN 1574-6968 ; 0378-1097
    ISSN (online) 1574-6968
    ISSN 0378-1097
    DOI 10.1111/j.1574-6968.2000.tb09183.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top