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1.

001-es BibID:BIBFORM071907
035-os BibID:(cikkazonosító)62 (WoS)000423384000001 (Scopus)85041107428
Első szerző:Agod Zsófia
Cím:Signaling Lymphocyte Activation Molecule Family 5 Enhances Autophagy and Fine-Tunes Cytokine Response in Monocyte-Derived Dendritic Cells via Stabilization of Interferon Regulatory Factor 8 / Zsofia Agod, Kitti Pazmandi, Dora Bencze, Gyorgy Vereb, Tamas Biro, Attila Szabo, Eva Rajnavolgyi, Attila Bacsi, Pablo Engel, Arpad Lanyi
Dátum:2018
ISSN:1664-3224
Megjegyzések:Signaling lymphocyte activation molecule family (SLAMF) receptors are essential regulators of innate and adaptive immune responses. The function of SLAMF5/CD84, a family member with almost ubiquitous expression within the hematopoietic lineage is poorly defined. In this paper we provide evidence that in human monocyte-derived dendritic cells (moDCs) SLAMF5 increases autophagy, a degradative pathway, which is highly active in dendritic cells (DCs) and plays a critical role in orchestration of the immune response. While investigating the underlying mechanism, we found that SLAMF5 inhibited proteolytic degradation of interferon regulatory factor 8 (IRF8) a master regulator of the autophagy process by a mechanism dependent on the E3 ubiquitin ligase tripartite motif-containing protein 21 (TRIM21). Furthermore, we demonstrate that SLAMF5 influences the ratio of CD1a+ cells in differentiating DCs and partakes in the regulation of IL?1?, IL?23 and IL?12 production in LPS/IFN??activated moDCs in a manner that is consistent with its effect on IRF8 stability. In summary, our experiments identified SLAMF5 as a novel cell surface receptor modulator of autophagy and revealed an unexpected link between the SLAMF and IRF8 signaling pathways, both implicated in multiple human pathologies.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
SLAMF5
Autophagy
Dendritic Cells
IRF8
TRIM21
IL?12p70
LPS/IFN?
Megjelenés:Frontiers in Immunology. - 9 (2018), p. 1-16. -
További szerzők:Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus) Bencze Dóra (1992-) Vereb György (1965-) (biofizikus, orvos) Bíró Tamás (1968-) (élettanász) Szabó Attila (1981-) (molekuláris biológus, immunológus, filozófus) Rajnavölgyi Éva (1950-) (immunológus) Bácsi Attila (1967-) (immunológus) Engel, Pablo Lányi Árpád (1962-) (biológus, immunológus)
Pályázati támogatás:NKFIH K 81676
Egyéb
NKFIH K 109444
Egyéb
Romanian Ministry of Education, Executive Agency For Higher Education, Research, Development and Innovation Funding, PNCDI II, project no. 119/2014
Egyéb
GINOP-2.3.2-15-2016-00050
GINOP
COST Action BM1404 Mye-EUNITER
Egyéb
János Bolyai Research Scholarship from the Hungarian Academy of Sciences
Egyéb
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2.

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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3.

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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4.

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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5.

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
TÁMOP
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6.

001-es BibID:BIBFORM065561
Első szerző:Bácsi Attila (immunológus)
Cím:Pathophysiology of bronchoconstriction : role of Oxidatively Damaged DNA Repair / Attila Bacsi, Lang Pan, Xueqing Ba, Istvan Boldogh
Dátum:2016
ISSN:1528-4050 1473-6322
Megjegyzések:PURPOSE OF REVIEW:To provide an overview on the present understanding of roles of oxidative DNA damage repair in cell signaling underlying bronchoconstriction common to, but not restricted to various forms of asthma and chronic obstructive pulmonary disease.RECENT FINDINGS:Bronchoconstriction is a tightening of smooth muscle surrounding the bronchi and bronchioles with consequent wheezing and shortness of breath. Key stimuli include air pollutants, viral infections, allergens, thermal and osmotic changes, and shear stress of mucosal epithelium, triggering a wide range of cellular, vascular, and neural events. Although activation of nerve fibers, the role of G-proteins, protein kinases and Ca++, and molecular interaction within contracting filaments of muscle are well defined, the overarching mechanisms by which a wide range of stimuli initiate these events are not fully understood. Many, if not all, stimuli increase levels of reactive oxygen species, which are signaling and oxidatively modifying macromolecules, including DNA. The primary reactive oxygen species target in DNA is guanine, and 8-oxoguanine is one of the most abundant base lesions. It is repaired by 8-oxoguanine DNA glycosylase1 during base excision repair processes. The product, free 8-oxo-7,8-dihydro-2'-deoxyguanosine base, is bound by 8-oxoguanine DNA glycosylase1 with high affinity, and the complex then functions as an activator of small guanosine triphosphatases, triggering pathways for inducing gene expression and contraction of intracellular filaments in mast and smooth muscle cells.SUMMARY:Oxidative DNA damage repair-mediated cell activation signaling result in gene expression that 'primes' the mucosal epithelium and submucosal tissues to generate mediators of airway smooth muscle contractions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
muscle constriction
oxidative DNA damage
8-oxoguanine DNA glycosylase1
small GTPases
Megjelenés:Current Opinion In Allergy And Clinical Immunology 16 : 1 (2016), p. 59-67. -
További szerzők:Pan, Lang Ba, Xueqing Boldogh István
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7.

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
Borító:

8.

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
Borító:

9.

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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10.

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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11.

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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12.

001-es BibID:BIBFORM035804
Első szerző:Bánhegyi Dénes
Cím:Significant decrease of the enhancement/neutralization index in HIV patients during highly active antiretroviral therapy (HAART) / Bánhegyi Dénes, Bácsi Attila, Tóth Ferenc D., Prohászka Zoltán, Horváth Anna, Beck Zoltán, Kónya József, Füst George
Dátum:2003
ISSN:0165-2478
Megjegyzések:Authors studied the effect of highly active antiretroviral therapy (HAART) on balance of the antibodies that enhance or neutralize growth of HIV-1(IIIB) strain in MT-4 cells in the presence or absence of human complement. Sequential serum samples were collected from 28 patients in advanced stage of HIV disease before and during HAART. The balance of the enhancing and neutralizing antibodies was expressed by an index value (E/N I). Samples with an E/N I of <0.5 (twofold decrease in virus production) were considered as neutralizing, whereas samples with an E/N I>2.0 (twofold increase in virus production) were considered as enhancing. At the beginning of HAART serum samples from eight patients enhanced, and samples from only two patients neutralized the virus in the presence of complement, median (25th-75th percentile) value of E/N I was 1.32 (0.79-2.29). E/N I significantly (P<0.0001) dropped to 0.37 (0.19-0.57) during the follow-up period of 18.5 (10.5-23.5) months under HAART. Similar changes were detected when serum samples were tested with no complement added. The E/N I values were also markedly decreased when cultures inoculated with mixtures of HIV and purified IgG prepared from serum pools taken before and during HAART, respectively, were compared. In the last samples of 20/28 patients, neutralization was measured even in the presence of complement while enhancement was found with none of these samples. These findings suggest that HAART results in disappearance of enhancing antibodies and switches the E/N I toward neutralization.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Immunology Letters. - 89 : 1 (2003), p. 25-30. -
További szerzők:Bácsi Attila (1967-) (immunológus) Tóth Ferenc, D. (1940-2004) (mikrobiológus, élettanász) Prohászka Zoltán Horváth Anna Beck Zoltán (1970-) (molekuláris biológus, mikrobiológus) Kónya József (1964-) (szakorvos, klinikai mikrobiológus) Füst György (Budapest)
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