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1.

001-es BibID:BIBFORM072833
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Pollen-induced oxidative DNA damage response regulates miRNAs controlling allergic inflammation / Aguilera-Aguirre Leopoldo, Hao Wenging, Pan Lang, Li Xiaoxue, Saavedra-Molina Alfredo, Bacsi Attila, Radak Zsolt, Sur Sanjiv, Brasier Allan R., Ba Xueqing, Boldogh Istvan
Dátum:2017
ISSN:1040-0605 1522-1504
Megjegyzések:A mucosal oxidative burst is a hallmark response to pollen exposure that promotes allergic inflammatory responses. Reactive species constituents of oxidative stress signal via the modification of cellular molecules including nucleic acids. One of the most abundant forms of oxidative genomic base damage is 8-oxo-7,8-dihydroguanine (8-oxoG), which is removed from DNA by 8-oxoguanine DNA glycosylase 1 (OGG1). OGG1 in complex with 8-oxoG acts as a GDP-GTP exchange factor and induces acute inflammation; however, the mechanism(s) by which OGG1 signaling regulates allergic airway inflammation is not known. Here, we postulate that the OGG1 signaling pathway differentially altered the levels of small regulatory RNAs and increased the expression of T helper 2 (Th2) cytokines in ragweed pollen extract (RWPE)-challenged lungs. To determine this, the lungs of sensitized mice expressing or lacking OGG1 were challenged with RWPE and/or with OGG1's excision product 8-oxoG. The responses in lungs were assessed by next-generation sequencing, as well as various molecular and histological approaches. The results showed that RWPE challenge induced oxidative burst and damage to DNA and activated OGG1 signaling, resulting in the differential expression of 84 micro-RNAs (miRNAs), which then exacerbated antigen-driven allergic inflammation and histological changes in the lungs. The exogenous administration of the downregulated let-7b-p3 mimetic or inhibitors of upregulated miR-23a or miR-27a decreased eosinophil recruitment and mucus and collagen production via controlling the expression of IL-4, IL-5, and IL-13. Together, these data demonstrate the roles of OGG1 signaling in the regulation of antigen-driven allergic immune responses via differential expression of miRNAs upstream of Th2 cytokines and eosinophils.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
DNA repair
allergy
cell signaling
micro-RNAs
Megjelenés:American Journal Of Physiology-Lung Cellular And Molecular Physiology 313 : 6 (2017), p. L1058-L1068. -
További szerzők:Hao, Wenging Pan, Lang Li, Xiaoxue Saavedra-Molina, Alfredo Bácsi Attila (1967-) (immunológus) Radák Zsolt Sur, Sanjiv Brasier, Allan R. Ba, Xueqing Boldogh István
Pályázati támogatás:OTKA-109595
OTKA
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2.

001-es BibID:BIBFORM065564
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Whole transcriptome analysis reveals a role for OGG1-initiated DNA repair signaling in airway remodeling / Leopoldo Aguilera-Aguirre, Koa Hosoki, Attila Bacsi, Zsolt Radák, Sanjiv Sur, Muralidhar L. Hegde, Bing Tian, Alfredo Saavedra-Molina, Allan R. Brasier, Xueqing Ba, Istvan Boldogh
Dátum:2015
ISSN:0891-5849
Megjegyzések:Reactive oxygen species (ROS) generated by environmental exposures, and endogenously as by-products of respiration, oxidatively modify biomolecules including DNA. Accumulation of ROS-induced DNA damage has been implicated in various diseases that involve inflammatory processes, and efficient DNA repair is considered critical in preventing such diseases. One of the most abundant DNA base lesions is 7,8-dihydro-8-oxoguanine (8-oxoG), which is repaired by the 8-oxoguanine DNA glycosylase 1 (OGG1)-initiated base-excision repair (OGG1-BER) pathway. Recent studies have shown that the OGG1-BER by-product 8-oxoG base forms a complex with cytosolic OGG1, activating small GTPases and downstream cell signaling in cultured cells and lungs. This implies that persistent OGG1-BER could result in signaling leading to histological changes in airways. To test this, we mimicked OGG1-BER by repeatedly challenging airways with its repair product 8-oxoG base. Gene expression was analyzed by RNA sequencing (RNA-Seq) and qRT-PCR, and datasets were evaluated by gene ontology and statistical tools. RNA-Seq analysis identified 3252 differentially expressed transcripts (2435 up- and 817 downregulated, ? 3-fold change). Among the upregulated transcripts, 2080 mRNAs were identified whose encoded protein products were involved in modulation of the actin family cytoskeleton, extracellular matrix, cell adhesion, cadherin, and cell junctions, affecting biological processes such as tissue development, cell-to-cell adhesion, cell communication, and the immune system. These data are supported by histological observations showing epithelial alterations, subepithelial fibrosis, and collagen deposits in the lungs. These data imply that continuous challenge by the environment and consequent OGG1-BER-driven signaling trigger gene expression consistent with airway remodeling.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
8-Oxoguanine
Airway remodeling
OGG1-BER
Megjelenés:Free Radical Biology And Medicine 89 (2015), p. 20-33. -
További szerzők:Hosoki, Koa Bácsi Attila (1967-) (immunológus) Radák Zsolt Sur, Sanjiv Hegde, Muralidhar L. Tian, Bing Saavedra-Molina, Alfredo Brasier, Allan R. Ba, Xueqing Boldogh István
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3.

001-es BibID:BIBFORM065605
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Whole transcriptome analysis reveals an 8-oxoguanine DNA glycosylase-1-driven DNA repair-dependent gene expression linked to essential biological processes / Leopoldo Aguilera-Aguirre, Koa Hosoki, Attila Bacsi, Zsolt Radák, Thomas G. Wood, Steven G. Widen, Sanjiv Sur, Bill T. Ameredes, Alfredo Saavedra-Molina, Allan R. Brasier, Xueqing Ba, Istvan Boldogh
Dátum:2015
ISSN:0891-5849
Megjegyzések:Reactiveoxygenspeciesinflict oxidativemodifications onvariousbiologicalmolecules,includingDNA.One ofthemostabundantDNAbaselesions,8-oxo-7,8-dihydroguanine(8-oxoG)isrepairedby8-oxoguanineDNAglycosylase-1(OGG1)duringDNAbaseexcisionrepair(OGG1-BER).8-OxoGaccumula-tion inDNAhasbeenassociatedwithvariouspathologicalandagingprocesses,althoughitsroleisunclear.ThelackofOGG1-BERin Ogg1 / mice resultedindecreasedinflammatory responsesandincreased susceptibilitytoinfectionsandmetabolicdisorders.Therefore,weproposedthatOGG1and/or8-oxoGbasemayhavearoleinimmuneandhomeostaticprocesses.Totestourhypothesis,wechallenged mouselungswithOGG1-BERproduct8-oxoGbaseandchangesingeneexpressionweredetermined byRNAsequencinganddatawereanalyzedbyGeneOntologyandstatisticaltools.RNA-Seqanalysisidentified 1592differentiallyexpressed(Z 3-fold change)transcripts.TheupregulatedmRNAswererelatedtobiologicalprocesses,includinghomeostatic,immune-system,macrophageactivation,regulation ofliquid-surfacetension,andresponsetostimulus.Theseprocessesweremediatedbychemokines, cytokines,gonadotropin-releasinghormonereceptor,integrin,andinterleukinsignalingpathways.Takentogether,these findings pointtoanewparadigmshowingthatOGG1-BERplaysarolein variousbiologicalprocessesthatmaybenefit thehost,butwheninexcesscouldbeimplicatedindisease and/oragingprocesses.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
OGG1-BER
8-Oxoguanine
Gene expression
Biological processes
Megjelenés:Free Radical Biology And Medicine. - 81 (2015), p. 107-118. -
További szerzők:Hosoki, Koa Bácsi Attila (1967-) (immunológus) Radák Zsolt Wood, Thomas G. Widen, Steven G. Sur, Sanjiv Ameredes, Bill T. Saavedra-Molina, Alfredo Brasier, Allan R. Ba, Xueqing Boldogh István
Pályázati támogatás:TAMOP4.2.2.A-11/1/KONV- 2012?2023
Egyéb
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4.

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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5.

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
TÁMOP
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6.

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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7.

001-es BibID:BIBFORM055556
035-os BibID:(scopus)84907867357 (wos)000343109700119
Első szerző:Ba, Xueqing
Cím:The Role of 8-Oxoguanine DNA Glycosylase-1 in Inflammation / Xueqing Ba, Leopoldo Aguilera-Aguirre, Qura Tul Ain Nmi Rashid, Attila Bacsi, Zsolt Radak, Sanjiv Sur, Koa Hosoki, Muralidhar L. Hegde, Istvan Boldogh
Dátum:2014
ISSN:1661-6596 1422-0067
Megjegyzések:Many, if not all, environmental pollutants/chemicals and infectious agents increase intracellular levels of reactive oxygen species (ROS) at the site of exposure. ROS not only function as intracellular signaling entities, but also induce damage to cellular molecules including DNA. Among the several dozen ROS-induced DNA base lesions generated in the genome, 8-oxo-7,8-dihydroguanine (8-oxoG) is one of the most abundant because of guanine's lowest redox potential among DNA bases. In mammalian cells, 8-oxoG is repaired by the 8-oxoguanine DNA glycosylase-1 (OGG1)-initiated DNA base excision repair pathway (OGG1-BER). Accumulation of 8-oxoG in DNA has traditionally been associated with mutagenesis, as well as various human diseases and aging processes, while the free 8-oxoG base in body fluids is one of the best biomarkers of ongoing pathophysiological processes. In this review, we discuss the biological significance of the 8-oxoG base and particularly the role of OGG1-BER in the activation of small GTPases and changes in gene expression, including those that regulate pro-inflammatory chemokines/cytokines and cause inflammation.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:International Journal of Molecular Sciences. - 15 : 9 (2014), p. 16975-16997. -
További szerzők:Aguilera-Aguirre, Leopoldo Rashid, Qura Tul Ain Nmi Bácsi Attila (1967-) (immunológus) Radák Zsolt Sur, Sanjiv Hosoki, Koa Hegde, Muralidhar L. Boldogh István
Pályázati támogatás:TAMOP 4.2.2.A-11/1/KONV-2012-2023
TÁMOP
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8.

001-es BibID:BIBFORM055861
Első szerző:Bácsi Attila (immunológus)
Cím:Plant pollens and molds directly induce oxidative stress in the airways / Bácsi Attila, Sur Sanjiv, Choudhury Barun, Hazra Tapas K., Boldogh István
Dátum:2002
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
Megjelenés:Free Radical Biology and Medicine. - 33 : Suppl. 2 (2002), p. 343. -
További szerzők:Sur, Sanjiv Choudhury, Barun K. Hazra, Tapas K. Boldogh István
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9.

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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10.

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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11.

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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12.

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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