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1.

001-es BibID:BIBFORM055870
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Oxidative damage to mitochondrial respiratory chain complexes increases allergic inflammation in mice / Aguilera-Aguirre Leopoldo, Saavedra-Molina Alfredo, Bácsi Attila, Sur Sanjiv, Boldogh István
Dátum:2007
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
Megjelenés:Journal of Allergy and Clinical Immunology. - 123 (2007), p. S122. -
További szerzők:Saavedra-Molina, Alfredo Bácsi Attila (1967-) (immunológus) Sur, Sanjiv Boldogh István
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2.

001-es BibID:BIBFORM055555
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Innate Inflammation Induced by the 8-Oxoguanine DNA Glycosylase-1-KRAS-NF-kB Pathway / Leopoldo Aguilera-Aguirre, Attila Bacsi, Zsolt Radak, Tapas K. Hazra, Sankar Mitra, Sanjiv Sur, Allan R. Brasier, Xueqing Ba, Istvan Boldogh
Dátum:2014
ISSN:0022-1767 1550-6606
Megjegyzések:8-Oxoguanine-DNA glycosylase-1 (OGG1) is the primary enzyme for repairing 7,8-dihydro-8-oxoguanine (8-oxoG) via the DNAbase excision repair pathway (OGG1-BER). Accumulation of 8-oxoG in the genomic DNA leads to genetic instability and carcinogenesis and is thought to contribute to the worsening of various inflammatory and disease processes. However, the disease mechanism is unknown. In this study, we proposed that the mechanistic link between OGG1-BER and proinflammatory gene expression is OGG1's guanine nucleotide exchange factor activity, acquired after interaction with the 8-oxoG base and consequent activationof the small GTPase RAS. To test this hypothesis, we used BALB/c mice expressing or deficient in OGG1 in their airwayepithelium and various molecular biological approaches, including active RAS pulldown, reporter and Comet assays, small interfering RNA?mediated depletion of gene expression, quantitative RT-PCR, and immunoblotting. We report that the OGG1-intiated repair of oxidatively damaged DNA is a prerequisite for GDP?GTP exchange, KRAS-GTP?driven signaling via MAP kinases and PI3 kinases and mitogen-stress?related kinase-1 for NF-kB activation, proinflammatory chemokine/cytokine expression, and inflammatory cell recruitment to the airways. Mice deficient in OGG1-BER showed significantly decreasedimmune responses, whereas a lack of other Nei-like DNA glycosylases (i.e., NEIL1 and NEIL2) had no significant effect. These data unveil a previously unidentified role of OGG1-driven DNA BER in the generation of endogenous signals for inflammation in the innate signaling pathway.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Immunology. - 193 : 9 (2014), p. 4643-4653. -
További szerzők:Bácsi Attila (1967-) (immunológus) Radák Zsolt Hazra, Tapas K. Mitra, Sankar Sur, Sanjiv Brasier, Allan R. Ba, Xueqing Boldogh István
Pályázati támogatás:TAMOP 4.2.2.A-11/1/KONV-2012-2023
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3.

001-es BibID:BIBFORM010166
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Mitochondrial dysfunction increases allergic airway inflammation / Leopoldo Aguilera-Aguirre, Attila Bácsi, Alfredo Saavedra-Molina, Alexander Kurosky, Sanjiv Sur, István Boldogh
Dátum:2009
Megjegyzések:The prevalence of allergies and asthma among the world's population has been steadily increasing due to environmental factors. It has been described that exposure to ozone, diesel exhaust particles, or tobacco smoke exacerbates allergic inflammation in the lungs. These environmental oxidants increase the levels of cellular reactive oxygen species (ROS) and induce mitochondrial dysfunction in the airway epithelium. In this study, we investigated the involvement of preexisting mitochondrial dysfunction in the exacerbation of allergic airway inflammation. After cellular oxidative insult induced by ragweed pollen extract (RWE) exposure, we have identified nine oxidatively damaged mitochondrial respiratory chain-complex and associated proteins. Out of these, the ubiquinol-cytochrome c reductase core II protein (UQCRC2) was found to be implicated in mitochondrial ROS generation from respiratory complex III. Mitochondrial dysfunction induced by deficiency of UQCRC2 in airway epithelium of sensitized BALB/c mice prior the RWE challenge increased the Ag-induced accumulation of eosinophils, mucin levels in the airways, and bronchial hyperresponsiveness. Deficiency of UQCRC1, another oxidative damage-sensitive complex III protein, did not significantly alter cellular ROS levels or the intensity of RWE-induced airway inflammation. These observations suggest that preexisting mitochondrial dysfunction induced by oxidant environmental pollutants is responsible for the severe symptoms in allergic airway inflammation. These data also imply that mitochondrial defects could be risk factors and may be responsible for severe allergic disorders in atopic individuals.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The Journal of Immunology. - 183 : 8 (2009), p. 5379-5387. -
További szerzők:Bácsi Attila (1967-) (immunológus) Saavedra-Molina, Alfredo Kurosky, Alexander Sur, Sanjiv Boldogh István
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4.

001-es BibID:BIBFORM011895
Első szerző:Almeida, Patrícia E.
Cím:Mycobacterium bovis bacillus Calmette-Guérin infection induces TLR2-dependent peroxisome proliferator-activated receptor gamma expression and activation : functions in inflammation, lipid metabolism, and pathogenesis / Patrícia E. Almeida, Adriana R. Silva, Clarissa M. Maya-Monteiro, Dániel Töröcsik, Heloisa D'Avila, Balázs Dezsö, Kelly G. Magalhaes, Hugo C. Castro-Faria-Neto, Laszlo Nagy, Patrícia T. Bozza
Dátum:2009
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The Journal of Immunology. - 183 : 2 (2009), p. 1337-1345. -
További szerzők:Silva, Adriana R. Maya-Monteiro, Clarissa M. Töröcsik Dániel (1979-) (bőrgyógyász) D'Avila Heloisa Dezső Balázs (1951-) (pathológus) Magalhaes, Kelly G. Castro-Faria-Neto, Hugo C. Nagy László (1966-) (molekuláris sejtbiológus, biokémikus) Bozza Patrícia T.
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5.

001-es BibID:BIBFORM004854
Első szerző:Andrásfalvy Márton
Cím:The beta subunit of the type I Fcepsilon receptor is a target for peptides inhibiting IgE-mediated secretory response of mast cells / Andrasfalvy, M., Peterfy, H., Toth, G., Matko, J., Abramson, J., Kerekes, K., Vamosi, G., Pecht, I., Erdei, A.
Dátum:2005
ISSN:0022-1767
Megjegyzések:Peptides originally derived from complement component C3a were earlier shown to inhibit the type I FcepsilonR (FcepsilonRI)-mediated degranulation of mucosal type mast cells. In the present study, we show that C3a7, a peptide with a natural sequence, and its modified derivative, C3a9, are powerful inhibitors of the above response of both serosal and mucosal type mastocytes. We demonstrate that these peptides inhibit FcepsilonRI-induced membrane proximal events, suppress phosphorylation of the FcepsilonRI beta subunit, the protein tyrosine kinase Lyn, as well as the transient rise in free cytosolic Ca2+ level. The late phase of cellular response was also inhibited, as demonstrated by the reduced TNF-alpha secretion. Experiments using two independent methods provided evidence that the interaction site of complement-derived peptides is the FcepsilonRI beta-chain. This was further supported by fluorescence confocal microscopic colocalization and resonance energy transfer measurements. Taken together, these results suggest the presence of distinct "activating" and "inhibitory" motifs in the C3a sequence. Response to both is in balance under physiologic conditions. Furthermore, present data predict that such inhibitory peptides may serve as potent agents for future therapeutic intervention.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
1-Phosphatidylinositol 3-Kinase
Animals
antagonists & inhibitors
Calcium
Cells
chemistry
Complement
Complement C3a
Energy Transfer
Fluorescence
Hungary
Immunoglobulin E
immunology
Mast Cells
metabolism
methods
Mice
Mice,Inbred BALB C
Necrosis
Oligopeptides
Peptides
pharmacology
Phosphorylation
physiology
Protein Subunits
Receptors,IgE
Research
secretion
Support
Tumor Necrosis Factor-alpha
Tyrosine
Megjelenés:The Journal of Immunology. - 175 : 5 (2005), p. 2801-2806. -
További szerzők:Péterfy Hajna Tóth Gábor (Szeged) Matkó János (1952-) (biológus) Abramson, Jakub Kerekes Krisztina Vámosi György (1967-) (biofizikus) Pecht, Israel Erdei Anna
Internet cím:elektronikus változat
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6.

001-es BibID:BIBFORM051534
035-os BibID:WOS:000332701400043
Első szerző:Ba, Xueqing
Cím:8-oxoguanine DNA glycosylase-1 augments proinflammatory gene expression by facilitating the recruitment of site-specific transcription factors / Xueqing Ba, Attila Bacsi, Jixian Luo, Leopoldo Aguilera-Aguirre, Xianlu Zeng, Zsolt Radak, Allan R. Brasier, Istvan Boldogh
Dátum:2014
ISSN:0022-1767 1550-6606
Megjegyzések:Among the insidious DNA base lesions, 8-oxo-7,8-dihydroguanine (8-oxoG) is one of the most abundant, a lesion that arises through the attack by reactive oxygen species on guanine, especially when located in cis-regulatory elements. 8-oxoG is repaired by the 8-oxoguanine glycosylase 1 (OGG1)-initiated DNA base excision repair pathway. In this study, we investigated whether 8-oxoG repair by OGG1 in promoter regions is compatible with a prompt gene expression and a host innate immune response. For this purpose, we used a mouse model of airway inflammation, supplemented with cell cultures, chromatin immunoprecipitation, small interfering RNA knockdown, real-time PCR, and comet and reporter transcription assays. Our data show that exposure of cells to TNF-? altered cellular redox, increased the 8-oxoG level in DNA, recruited OGG1 to promoter sequences, and transiently inhibited base excision repair of 8-oxoG. Promoter-associated OGG1 then enhanced NF-?B/RelA binding to cis-elements and facilitated recruitment of specificity protein 1, transcription initiation factor II-D, and p-RNA polymerase II, resulting in the rapid expression of chemokines/cytokines and inflammatory cell accumulation in mouse airways. Small interfering RNA depletion of OGG1 or prevention of guanine oxidation significantly decreased TNF-?-induced inflammatory responses. Taken together, these results show that nonproductive binding of OGG1 to 8-oxoG in promoter sequences could be an epigenetic mechanism to modulate gene expression for a prompt innate immune response.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
OGG1
8-oxoG
trans-ACTING FACTORS
INNATE IMMUNE RESPONSE
Megjelenés:Journal of Immunology. - 192 : 5 (2014), p. 2384-2394. -
További szerzők:Bácsi Attila (1967-) (immunológus) Luo, Jixian Aguilera-Aguirre, Leopoldo Zeng, Xianlu Radák Zsolt Brasier, Allan R. Boldogh István
Pályázati támogatás:4.2.2.A-11/1/KONV-2012-0023
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7.

001-es BibID:BIBFORM053872
Első szerző:Bachmann, Michael
Cím:Autoimmunity as a result of escape from RNA surveillance / Michael P. Bachmann, Holger Bartsch, Joanne K. Gross, Shannon M. Maier, Timothy F. Gross, Jennifer L. Workman, Judith A. James, A. Darise Farris, Bettina Jung, Claudia Franke, Karsten Conrad, Marc Schmitz, Cordula Büttner, Jill P. Buyon, Imre Semsei, John B. Harley, E. Peter Rieber
Dátum:2006
ISSN:0022-1767 1550-6606
Megjegyzések:In previous studies, we detected a frame shift mutation in the gene encoding the autoantigen La of a patient with systemic lupus erythematosus. The mutant La mRNA contains a premature termination codon. mRNAs that prematurely terminate translation should be eliminated by RNA quality control mechanisms. As we find Abs specific for the mutant La form in approximately 30% of sera from anti-La-positive patients, we expected that mutant La mRNAs circumvent RNA control and the expression of mutant La protein could become harmful. Indeed, real-time PCR, immunostaining, and immunoblotting data of mice transgenic for the mutant La form show that mutant La mRNAs are not repressed in these animals and are translated to mutant La protein. In addition to the mutant La protein, we detected a minor portion of native human La in the mutant La-transgenic mice. Therefore, ribosomal frame shifting may allow the mutant La mRNA to escape from RNA control. Interestingly, expression of the mutant La mRNA results in a lupus-like disease in the experimental mice. Consequently, escape of mutant La mRNA from RNA control can have two effects: it 1) results in the expression of an immunogenic (neo)epitope, and 2) predisposes to autoimmunity.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Immunology. - 177 : 3 (2006), p. 1698-1707. -
További szerzők:Bartsch, Holger Gross, Joanne K. Maier, Shannon Gross, Timothy F. Workman, Jennifer L. James, Judith A. Farris, Darise Jung, Bettina Franke, Claudia Conrad, Karsten Schmitz, Marc Buttner, Cordula Buyon, Jill P. Semsei Imre (1954-) (vegyész, gerontológus) Harley, John B. Rieber, E. Peter
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8.

001-es BibID:BIBFORM055863
Első szerző:Bácsi Attila (immunológus)
Cím:Pro-oxidant activity of pollen and mold proteins induces oxidative stress in the lungs independent of adaptive immunity / Bácsi Attila, Sur Sanjiv, Choudhury Barun K., Alam Rafeul, Boldogh István
Dátum:2003
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
Megjelenés:Journal of Allergy and Clinical Immunology. - 111 : Suppl. 1 (2003), p. S340. -
További szerzők:Sur, Sanjiv Choudhury, Barun K. Alam, Rafeul Boldogh István
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9.

001-es BibID:BIBFORM055866
Első szerző:Bácsi Attila (immunológus)
Cím:Reactive Oxygen Species Generated by Pollen Grain's NAD(P)H Oxidase Augment Allergic Ocular Symptoms / Bácsi Attila, Dharajiya Nilesh, Choudhury Barun K., Sur Sanjiv, Boldogh István
Dátum:2004
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
Megjelenés:Journal of Allergy and Clinical Immunology. - 113 : Suppl. 2. (2004), p. S164. -
További szerzők:Dharajiya, Nilesh G. Choudhury, Barun K. Sur, Sanjiv Boldogh István
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10.

001-es BibID:BIBFORM055871
Első szerző:Bácsi Attila (immunológus)
Cím:Antigen-independent mitochondria-driven release of biogenic amines from RBL-2H3 cells / Bácsi Attila, Chodaczek Grzegorz, Dharajiya Nilesh, Sur Sanjiv, Hazra Tapas K., Boldogh István
Dátum:2007
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
Megjelenés:Journal of Allergy and Clinical Immunology. - 123 (2007), p. S118. -
További szerzők:Chodaczek, Grzegorz Dharajiya, Nilesh G. Sur, Sanjiv Hazra, Tapas K. Boldogh István
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11.

001-es BibID:BIBFORM047645
035-os BibID:PMID:16210058
Első szerző:Bácsi Attila (immunológus)
Cím:Effect of pollen-mediated oxidative stress on immediate hypersensitivity reactions and late-phase inflammation in allergic conjunctivitis / Attila Bacsi, Nilesh Dharajiya, Barun K. Choudhury, Sanjiv Sur, Istvan Boldogh
Dátum:2005
ISSN:0091-6749
Megjegyzések:BACKGROUND:Allergic eye diseases are complex inflammatory conditions of the conjunctiva that are becoming increasingly prevalent and present an increasing economic burden because of direct and indirect health expenditures.OBJECTIVE:We sought to identify factors that may synergize with antigen-induced allergic inflammation and lead to allergic conjunctivitis. We used a murine model of allergic conjunctivitis to test the effect of oxidative stress generated by pollen oxidases using nicotinamide adenine dinucleotide (reduced) or nicotinamide adenine dinucleotide phosphate (reduced) (NAD[P]H) as an electron donor present in pollen grains.METHODS:Reactive oxygen species (ROS) generation by hydrated Ambrosia artemisiifolia pollen (short ragweed pollen; RWP) grains was determined by using 2'-7'-dihydro-dichlorofluorescein diacetate, nitroblue tetrazolium reduction, and Amplex Red assay. The RWP-induced changes in intracellular ROS levels were examined in A549 cells, human primary bronchial epithelial cells, and murine conjunctiva.RESULTS:Ragweed pollen grains contain NAD(P)H oxidase activity, which is diphenyleneiodonium-sensitive and quinacrine-sensitive and sodium azide-resistant. These NAD(P)H oxidases generate a superoxide anion that can be converted to H2O2 by pollen grain-associated superoxide dismutase. These diffusible oxygen radicals from pollen grains increase intracellular ROS levels in cultured epithelial cells and murine conjunctiva. Similar phenomena were observed in sensitized and naive mice, indicating that the RWP-induced oxidative stress in conjunctival epithelium is independent of adaptive immunity. Inactivation of NAD(P)H oxidase activity in RWP decreases the immediate-type hypersensitivity and inflammatory cell infiltration into the conjunctiva.CONCLUSION:Our data suggest that ROS generated by NAD(P)H oxidases in pollen grains intensify immediate allergic reactions and recruitment of inflammatory cells in murine conjunctiva.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Pollen NAD(P)H oxidase
oxidative stress
epithelium
conjunctivitis
Megjelenés:Journal of Allergy and Clinical Immunology. - 116 : 4 (2005), p. 836-843. -
További szerzők:Dharajiya, Nilesh G. Choudhury, Barun K. Sur, Sanjiv Boldogh István
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12.

001-es BibID:BIBFORM038720
Első szerző:Bácsi Attila (immunológus)
Cím:Subpollen particles : carriers of allergenic proteins and oxidases / Bacsi A., Choudhury B.K., Dharajiya N., Sur S., Boldogh I.
Dátum:2006
ISSN:0091-6749
Megjegyzések:Pollen is known to induce allergic asthma in atopic individuals, although only a few inhaled pollen grains penetrate into the lower respiratory tract. OBJECTIVE: We sought to provide evidence that subpollen particles (SPPs) of respirable size, possessing both antigenic and redox properties, are released from weed pollen grains and to test their role in allergic airway inflammation. METHODS: The release of SPPs was analyzed by means of microscopic imaging and flow cytometry. The redox properties of SPPs and the SPP-mediated oxidative effect on epithelial cells were determined by using redox-sensitive probes and specific inhibitors. Western blotting and amino acid sequence analysis were used to examine the protein components of the SPP. The allergenic properties of the SPP were determined in a murine model of experimental asthma. RESULTS: Ragweed pollen grains released 0.5 to 4.5 microm of SPPs on hydration. These contained Amb a 1, along with other allergenic proteins of ragweed pollen, and possessed nicotinamide adenine dinucleotide (reduced) or nicotinamide adenine dinucleotide phosphate (reduced) [NAD(P)H] oxidase activity. The SPPs significantly increased the levels of reactive oxygen species (ROS) in cultured cells and induced allergic airway inflammation in the experimental animals. Pretreatment of the SPPs with NAD(P)H oxidase inhibitors attenuated their capacity to increase ROS levels in the airway epithelial cells and subsequent airway inflammation. CONCLUSIONS: The allergenic potency of SPPs released from ragweed pollen grains is mediated in tandem by ROS generated by intrinsic NAD(P)H oxidases and antigenic proteins.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Allergy And Clinical Immunology. - 118 : 4 (2006), p. 844-850. -
További szerzők:Choudhury, Barun K. Dharajiya, Nilesh G. Sur, Sanjiv Boldogh István
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