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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
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM041840
Első szerző:	Murai, Hiroki
Cím:	Alternaria-Induced Release of IL-18 from Damaged Airway Epithelial Cells : n NF-kB Dependent Mechanism of Th2 Differentiation? / Hiroki Murai, Huibin Qi, Barun Choudhury, Jim Wild, Nilesh Dharajiya, Swapnil Vaidya, Anjana Kalita, Attila Bacsi, David Corry, Alexander Kurosky, Allan Brasier, Istvan Boldogh, Sanjiv Sur
Dátum:	2012
Megjegyzések:	BACKGROUND: A series of epidemiologic studies have identified the fungus Alternaria as a major risk factor for asthma. The airway epithelium plays a critical role in the pathogenesis of allergic asthma. These reports suggest that activated airway epithelial cells can produce cytokines such as IL-25, TSLP and IL-33 that induce Th2 phenotype. However the epithelium-derived products that mediate the pro-asthma effects of Alternaria are not well characterized. We hypothesized that exposure of the airway epithelium to Alternaria releasing cytokines that can induce Th2 differentiation.METHODOLOGY/PRINCIPAL FINDING: We used ELISA to measure human and mouse cytokines. Alternaria extract (ALT-E) induced rapid release of IL-18, but not IL-4, IL-9, IL-13, IL-25, IL-33, or TSLP from cultured normal human bronchial epithelial cells; and in the BAL fluids of naïve mice after challenge with ALT-E. Both microscopic and FACS indicated that this release was associated with necrosis of epithelial cells. ALT-E induced much greater IL-18 release compared to 19 major outdoor allergens. Culture of naïve CD4 cells with rmIL-18 induced Th2 differentiation in the absence of IL-4 and STAT6, and this effect was abrogated by disrupting NF- ?B p50 or with a NEMO binding peptide inhibitor.CONCLUSION/SIGNIFICANCE: Rapid and specific release of IL-18 from Alternaria-exposed damaged airway epithelial cells can directly initiate Th2 differentiation of naïve CD4(+) T-cells via a unique NF-?B dependent pathway.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	PLoS One. - 7 : 2 (2012), p. e30280. -
További szerzők:	Qi, Huibin Choudhury, Barun K. Wild, Jim Dharajiya, Nilesh G. Vaidya, Swapnil Kalita, Anjana Bácsi Attila (1967-) (immunológus) Corry, David Kurosky, Alexander Brasier, Allan R. Boldogh István Sur, Sanjiv
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM047650
Első szerző:	Woodberry, Mitchell
Cím:	ATP Depletion Via Mitochondrial F1F0 Complex by Lethal Factor is an Early Event in B. Anthracis-Induced Sudden Cell Death / Mitchell W. Woodberry, Leopoldo Aguilera-Aguirre, Attila Bacsi, Ashok K. Chopra, Alexander Kurosky, Johnny W. Peterson, Istvan Boldogh
Dátum:	2009
Megjegyzések:	Bacillus anthracis' primary virulence factor is a tripartite anthrax toxin consisting of edema factor (EF), lethal factor (LF)and protective antigen (PA). In complex with PA, EF and LF are internalized via receptor-mediated endocytosis. EF is a calmodulindependentadenylate cyclase that induces tissue edema. LF is a zinc-metalloprotease that cleaves members of mitogen-activated proteinkinase kinases. Lethal toxin (LT: PA plus LF)-induced death of macrophages is primarily attributed to expression of the sensitiveNalp1b allele, inflammasome formation and activation of caspase-1, but early events that initiate these processes are unknown. Herewe provide evidence that an early essential event in pyroptosis of alveolar macrophages is LF-mediated depletion of cellular ATP. Theunderlying mechanism involves interaction of LF with F1F0-complex gamma and beta subunits leading to increased ATPase activity inmitochondria. In support, mitochondrial DNA-depleted MH-S cells have decreased F1F0 ATPase activity due to the lack of F06 and F08polypeptides and show increased resistance to LT. We conclude that ATP depletion is an important early event in LT-induced sudden celldeath and its prevention increases survival of toxin-sensitive cells.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban anthrax lethal factor mitochondria F1F0 ATPase pyroptosis
Megjelenés:	Journal of Cell Death. - 2 (2009), p. 25-39. -
További szerzők:	Aguilera-Aguirre, Leopoldo Bácsi Attila (1967-) (immunológus) Chopra, Ashok K. Kurosky, Alexander Peterson, Johnny W. Boldogh István
Internet cím:	Szerző által megadott URL Intézményi repozitóriumban (DEA) tárolt változat
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