CCL

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1.

001-es BibID:BIBFORM047649
Első szerző:Bácsi Attila (immunológus)
Cím:Colostrinin decreases spontaneous and induced mutation frequencies at the hprt locus in Chinese hamster V79 cells / Attila Bacsi, Leopoldo Aguilera-Aguirre, Peter German, Marian L. Kruzel, Istvan Boldogh
Dátum:2006
Megjegyzések:ColostrininTM (CLN), a uniform mixture of lowmolecular weight, proline-rich polypeptides, induces neurite outgrowth of pheochromocytoma cells, extends the lifespan of diploid fibroblast cells, inhibits beta amyloid-induced apoptosis and resulted in improved cognitive function when administered to Alzheimer's patients. Here we investigated CLN's antimutagenic activity in cells stressed oxidatively or exposed to chemical or physical agents. Our data show that CLN did not alter cell cycle kinetics and cloning efficiency, while it inhibited the development of spontaneous mutations at the coding region of the hypoxanthine phosphoribosyl-transferase (hprt) gene in Chinese hamster V79 cells. In a dosedependent manner, CLN lowered reactive oxygen species (ROS)-induced frequency of cells resistant to 6-thioguanine (6-TG) to nearly background level. Likewise, CLN decreased the frequency of methyl methanesulfonate- or mitomycin C-induced mutations in V79 cells. Notably, CLN (at 100, 250, and 500 ng per ml concentrations) decreased UVAinduced mutation frequency, while only the highest dose of CLN also decreased significantly the number of UVB-induced 6-TG-resistant mutant cells. Similar results were obtained using cell cultures of human origin. Overall, our data show that CLN significantly lowers the mutation frequency that develops spontaneously or is induced by ROS, chemical and physical agents. CLN itself has no mutagenic activity. Therefore, CLN may be used in human therapies systemically and/or locally for the prevention of diseases associated with sequence alterations in genomic and mitochondrial DNA.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
colostrinin
mutation frequency
oxidative stress
genotoxic chemical and physical agents
Megjelenés:Journal of Experimental Therapeutics and Oncology 5 : 4 (2006), p. 249-259. -
További szerzők:Aguilera-Aguirre, Leopoldo Germán Péter (gyermekgyógyász) Kruzel, Marian L. Boldogh István
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2.

001-es BibID:BIBFORM047648
Első szerző:Bácsi Attila (immunológus)
Cím:Colostrinin-Driven Neurite Outgrowth Requires p53 Activation in PC12 Cells / Attila Bacsi, G. John Stanton, Thomas K. Hughes, Marian Kruzel, Istvan Boldogh
Dátum:2005
ISSN:0272-4340
Megjegyzések:1. Colostrinin (CLN) induces maturation and differentiation of murine thymocytes,promotes proliferation of peripheral blood leukocytes, induces immunomodulatorcytokines, and ameliorates oxidative stress-mediated activation of c-Jun NH2-terminalkinases.2. Here we report that upon treatment with CLN, medullary pheochromocytoma(PC12) cells ceased to proliferate and extend neurites.3. The arrest of CLN-treated PC12 cells in the G1 phase of the cell cycle was due toan increase in the phosphorylation of p53 at serine15 (p53ser15) and expression of p21WAF1.PC12 cells treated with inhibitory oligonucleotides to p53 lacked p53ser15 and p21WAF1expression, and did not show morphological changes after CLN exposure. Transfectionwith inhibitory oligonucleotides to p21WAF1 had no effect on p53 activation; however, cellsfailed to arrest or extend neurites. An oligonucleotide inhibiting luciferase expression hadno effect on CLN-mediated p53 activation, p21WAF1 expression, growth arrest, or neuriteoutgrowth.4. We conclude that CLN induces delicate cassettes of signaling pathways common tocell proliferation and differentiation, and mediates activities that are similar to those ofhormones and neurotrophins, leading to neurite outgrowth.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
colostrinin
pheochromocytoma cell
neurite outgrowth
p53 activation
Megjelenés:Cellular And Molecular Neurobiology. - 25 : 7 (2005), p. 1123-1139. -
További szerzők:Stanton, G. John Hughes, Thomas K. Kruzel, Marian L. Boldogh István
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3.

001-es BibID:BIBFORM002002
Első szerző:Bácsi Attila (immunológus)
Cím:Colostrinin delays the onset of proliferative senescence of diploid murine fibroblast cells / Attila Bacsi, Mitchell Woodberry, Marian L. Kruzel, Istvan Boldogh
Dátum:2007
Megjegyzések:Colostrinine (CLN), a uniform mixture of low-molecular weight, proline-rich polypeptides, induces neurite outgrowth of pheochromocytoma cells and inhibits beta amyloid-induced apoptosis. Moreover, its administration to patients with Alzheimer's disease resulted in improved cognitive functions. In this study, we investigated the impact of CLN on the lifespan of murine diploid fibroblast cells (MDF), an in vitro model for cellular aging. Here, we show that CLN significantly decelerates the senescence of cultured MDF and increases their population doubling levels. This action of CLN is associated with a decrease in the intracellular levels of reactive oxygen species, which may be due to senescence-associated mitochondrial dysfunction. These data suggest that CLN may delay the development of cellular aging at the level of the organism. Thus, CLN may be used in the prevention and/or therapy of diseases associated with aging processes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Colostrinine
Oxidative stress
Lifespan
Megjelenés:Neuropeptides. - 41 : 2 (2007), p. 93-101. -
További szerzők:Woodberry, Mitchell Kruzel, Marian L. Boldogh István
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4.

001-es BibID:BIBFORM055868
Első szerző:Boldogh István
Cím:Colostrinin (TM) increases the lifespan and neurological performance of mice / Boldogh I., Bácsi A., Agulera-Aguirre L., Germán P., Kruzel M.
Dátum:2008
Tárgyszavak:Természettudományok Biológiai tudományok előadáskivonat
Megjelenés:New Trends in Alzheimer and Parkinson Related Disorders : ADPD 2007 / eds. Hanin I., Windisch M., Poewe W., Fisher A. - [1] p. -
További szerzők:Bácsi Attila (1967-) (immunológus) Aguilera-Aguirre, Leopoldo Germán Péter (gyermekgyógyász) Kruzel, Marian L.
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5.

001-es BibID:BIBFORM006107
Első szerző:Boldogh István
Cím:Colostrinin decreases hypersensitivity and allergic responses to common allergens / Istvan Boldogh, Leopoldo Aguilera-Aguirre, Attila Bacsi, Barun K. Choudhury, Alfredo Saavedra-Molina, Marian Kruzel
Dátum:2008
Megjegyzések:Colostrinin (TM) (CLN), isolated from mothers' pre-milk fluid (colostrum), is a uniform mixture of low-molecular-weight, proline-rich polypeptides. CLN induces neurite outgrowth of pheochromocytoma cells, extends the lifespan of diploid fibroblast cells, inhibits beta-amyloid-induced apoptosis and improves cognitive functions when administered to Alzheimer's disease patients. Objective: The aim of this study was to investigate potential allergic responses to CLN and its impact on allergic sensitization and inflammation caused by common allergens. Methods: We used a well-characterized mouse model of allergic airway inflammation. Changes in IgE/IgG1 and mucin levels, airway eosinophilia and hyperreactivity to methacholine were determined by ELISA, differential cell counting and whole-body plethysmography, respectively. Results: CLN did not increase IgE/IgG1 levels or induce cutaneous hypersensitivity reaction, airway inflammation and mucin production. Importantly, CLN significantly (p < 0.001) decreased IgE/IgG1 production, airway eosinophilia, mucin production and hypersensitivity induced by allergenic extracts from ragweed pollen grains and house dust mites. Conclusion: CLN itself is non-allergenic; however, it is effective in preventing allergic responses to known indoor and outdoor allergens. These data support the safe application of CLN and its potential use in the prevention of allergic inflammation in humans.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
colostrinin
immunoglobulin E
allergic inflammation
Megjelenés:International Archives of Allergy and Immunology. - 146 : 4 (2008), p. 298-306. -
További szerzők:Aguilera-Aguirre, Leopoldo Bácsi Attila (1967-) (immunológus) Choudhury, Barun K. Saavedra-Molina, Alfredo Kruzel, Marian L.
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6.

001-es BibID:BIBFORM002001
Első szerző:Chodaczek, Grzegorz
Cím:Iron-mediated dismutation of superoxide anion augments antigen-induced allergic inflammation : effect of lactoferrin / Grzegorz Chodaczek, Alfredo Saavedra-Molina, Attila Bacsi, Marian L. Kruzel, Sanjiv Sur, Istvan Boldogh
Dátum:2007
Megjegyzések:The authors previously showed that pollen grain-, pollen grain extract-. and subpollen particle-induced allergic inflammation in lungs and eyes is robustly augmented by their intrinsic NAD(P)H oxidase activity. Here they sought to determine whether lactoferrin (LF), an iron-binding protein and immune modulator, decreases allergic inflammation induced by ragweed (Ambrosia artemisiifolia) pollen grain extract (RWE). MATERIAL/METHODS: The impact of LF on NAD(P)H oxidase in pollen grains and reactive oxygen species (ROS) levels in vitro and in the lungs of experimental animals was assessed by use of redox-sensitive probes and specific inhibitors. The influence of LF on RWE-induced allergic inflammation was determined in a mouse experimental model of asthma. RESULTS: The data show that the intrinsic NAD(P)H oxidase of pollen grains generates superoxide anion (O2-) and that LF does not alter its enzymatic activity, as shown by nitroblue tetrazolium and cytochrome c assays. On the other hand, LF significantly decreased H(2)- O(2)- and lipid peroxide (4-hydroxynoneal and malondialdehyde) levels in airway lining fluids and lung epithelium after intranasal challenge of naive or sensitized mice with RWE. Furthermore, a single dose of LF prevented/decreased the abundance of the RWE-induced robust accumulation of inflammatory and mucin-producing cells in airways and subepithelial compartments and decreased airway hyperreactivity. CONCLUSION: These data suggest that the reduced conversion of NAD(P)H oxidase-generated O(2)- into H(2)- O(2)- and/or OH, which in turn synergistically enhanced pollen antigen-induced airway inflammation, is due to the iron-binding capacity of LF. These results support the utility of LF in human allergic inflammatory disorders.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Lactoferrin
allergy
airway infl ammation
oxidative stress
Megjelenés:Postepy higieny i medycyny doswiadczalnej (Online). - 61 (2007), p. 268-278. -
További szerzők:Saavedra-Molina, Alfredo Bácsi Attila (1967-) (immunológus) Kruzel, Marian L. Sur, Sanjiv Boldogh István
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7.

001-es BibID:BIBFORM040234
Első szerző:Kruzel, Marian L.
Cím:Lactoferrin decreases pollen antigen-induced allergic airway inflammation in a murine model of asthma / Kruzel M.L., Bacsi A., Choudhury B., Sur S., Boldogh I.
Dátum:2006
ISSN:0019-2805
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Immunology. - 119 : 2 (2006), p. 159-166. -
További szerzők:Bácsi Attila (1967-) (immunológus) Choudhury, Barun K. Sur, Sanjiv Boldogh István
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8.

001-es BibID:BIBFORM014050
Első szerző:Kruzel, Marian L.
Cím:Lactoferrin decreases LPS-induced mitochondrial dysfunction in cultured cells and in animal endotoxemia model / Marian L. Kruzel, Jeffrey K. Actor, Zsolt Radak, Attila Bacsi, Alfredo Saavedra-Molina, Istvan Boldogh
Dátum:2010
ISSN:1753-4259
Megjegyzések:Lactoferrin is a non-heme iron-binding glycoprotein, produced by mucosal epithelial cells and granulocytes in most mammalian species. It is involved in regulation of immune responses, possesses anti-oxidant, anti-carcinogenic, anti-inflammatory properties, and provides protection against various microbial infections. In addition, lactoferrin has been implicated in protection against the development of insult-induced systemic inflammatory response syndrome (SIRS) and its progression into septic conditions in vivo. Here we show a potential mechanism by which lactoferrin lessens oxidative insult at the cellular and tissue levels after lipopolysaccharide (LPS) exposure. Lactoferrin pretreatment of cells decreased LPS-mediated oxidative insults in a dose-dependent manner. Lipopolysaccharide-induced oxidative burst was found to be of mitochondrial origin, and release of reactive oxygen species (ROS) was localized to the respiratory complex III. Importantly, lactoferrin nearly abolished LPS-induced increases in mitochondrial ROS generation and the accumulation of oxidative damage in the DNA. In vivo, pretreatment of experimental animals with lactoferrin significantly (P50.05) lowered LPS-induced mitochondrial dysfunction as shown by both decreased release of H2O2 and DNA damage in the mitochondria. In contrast, deferoxamine, an iron chelating compound, provided only partial protection in LPS-treated animals. Together, these data suggest that lactoferrin protects against oxidative insult at the mitochondrial level, and indicate a potential utility of lactoferrin in prevention and treatment of SIRS.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
DNA-DAMAGE
HYDROGEN-PEROXIDE
OXIDATIVE DAMAGE
ROS GENERATION
REPAIR
MECHANISMS
OXIDASES
SEPSIS
DEATH
MTDNA
Megjelenés:Innate Immunity 16 : 2 (2010), p. 67-79. -
További szerzők:Actor, Jeffrey K. Radák Zsolt Bácsi Attila (1967-) (immunológus) Saavedra-Molina, Alfredo Boldogh István
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