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001-es BibID:BIBFORM098738
035-os BibID:(cikkazonosító)630569 (WoS)000627757800001 (Scopus)85102440838
Első szerző:Alatshan, Ahmad (immunológus)
Cím:Nuclear Receptors as Multiple Regulators of NLRP3 Inflammasome Function / Alatshan Ahmad, Benkő Szilvia
Dátum:2021
ISSN:1664-3224
Megjegyzések:Nuclear receptors are important bridges between lipid signaling molecules and transcription responses. Beside their role in several developmental and physiological processes, many of these receptors have been shown to regulate and determine the fate of immune cells, and the outcome of immune responses under physiological and pathological conditions. While NLRP3 inflammasome is assumed as key regulator for innate and adaptive immune responses, and has been associated with various pathological events, the precise impact of the nuclear receptors on the function of inflammasome is hardly investigated. A wide variety of factors and conditions have been identified as modulators of NLRP3 inflammasome activation, and at the same time, many of the nuclear receptors are known to regulate, and interact with these factors, including cellular metabolism and various signaling pathways. Nuclear receptors are in the focus of many researches, as these receptors are easy to manipulate by lipid soluble molecules. Importantly, nuclear receptors mediate regulatory mechanisms at multiple levels: not only at transcription level, but also in the cytosol via non-genomic effects. Their importance is also reflected by the numerous approved drugs that have been developed in the past decade to specifically target nuclear receptors subtypes. Researches aiming to delineate mechanisms that regulate NLRP3 inflammasome activation draw a wide range of attention due to their unquestionable importance in infectious and sterile inflammatory conditions. In this review, we provide an overview of current reports and knowledge about NLRP3 inflammasome regulation from the perspective of nuclear receptors, in order to bring new insight to the potentially therapeutic aspect in targeting NLRP3 inflammasome and NLRP3 inflammasome-associated diseases.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
inflammasome
NLRP3
IL-1
signaling
PPAR
LXR
PXR
metabolism
Megjelenés:Frontiers in Immunology. - 12 (2021), p. 630569. -
További szerzők:Benkő Szilvia (1973-) (molekuláris biológus)
Pályázati támogatás:K131844
OTKA
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2.

001-es BibID:BIBFORM086920
035-os BibID:(cikkazonosító)1591 (WoS)000554261900001 (Scopus)85087733361
Első szerző:Alatshan, Ahmad (immunológus)
Cím:All-Trans Retinoic Acid Enhances both the Signaling for Priming and the Glycolysis for Activation of NLRP3 Inflammasome in Human Macrophage / Ahmad Alatshan, Gergő E. Kovács, Azzam Aladdin, Zsolt Czimmerer, Krisztina Tar, Szilvia Benkő
Dátum:2020
ISSN:2073-4409
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Cells. - 9 : 7 (2020), p. 1591. -
További szerzők:Kovács Gergő E. Aladdin, Azzam (1980-) (molekuláris biológus) Czimmerer Zsolt (1981-) (molekuláris biológus) Tar Krisztina (1975-) (biokémikus, molekuláris biológus) Benkő Szilvia (1973-) (molekuláris biológus)
Pályázati támogatás:NKFIH-OTKA 131844
OTKA
OTKA FK132185
OTKA
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM081504
035-os BibID:(PMID)31134061 (cikkazonosító)937 (WoS)000466465900001 (Scopus)85067055685
Első szerző:Csete Dániel
Cím:Hematopoietic or Osteoclast-Specific Deletion of Syk Leads to Increased Bone Mass in Experimental Mice / Dániel Csete, Edina Simon, Ahmad Alatshan, Petra Aradi, Csaba Dobó-Nagy, Zoltán Jakus, Szilvia Benkő, Dávid S. Győri, Attila Mócsai
Dátum:2019
ISSN:1664-3224
Megjegyzések:Syk is a non-receptor tyrosine kinase critically involved in signaling by various immunoreceptors including B-cell-receptors and activating Fc-receptors. We have previously shown that Syk also mediates immunoreceptor-like signals required for the in vitro development and function of osteoclasts. However, the perinatal lethality of Syk -/- mice precluded the analysis of the role of Syk in in vivo bone metabolism. To overcome that problem, we generated mice with osteoclast-specific (Syk ?OC ) or hematopoietic (Syk ?Haemo ) Syk deficiency by conditional deletion of Syk using Cre recombinase expressed under the control of the Ctsk or Vav1 promoter, respectively. Micro-CT analysis revealed increased bone trabecular density in both Syk ?OC and Syk ?Haemo mice, although hematopoietic Syk deficiency caused a more severe phenotype than osteoclast-specific Syk deficiency. Osteoclast-specific Syk deficiency reduced, whereas hematopoietic Syk deficiency completely blocked in vitro development of osteoclasts. Both interventions inhibited the resorptive activity of osteoclasts and osteoclast-specific gene expression. Kinetic analysis of Syk protein levels, Cre expression and the genomic deletion of the Syk flox allele revealed complete and early deletion of Syk from Syk ?Haemo osteoclasts whereas Syk was incompletely deleted at a later stage of osteoclast development from Syk ?OC cultures. Those results provide an explanation for the in vivo and in vitro difference between the Syk ?OC and Syk ?Haemo mutant strains and suggest late activation of, and incomplete target gene deletion upon, osteoclast-specific Cre expression driven by the Ctsk promoter. Taken together, our results indicate that Syk plays an indispensable role in osteoclast-mediated in vivo bone resorption and suggest that Syk-specific inhibitors may provide therapeutic benefit in inflammatory and other diseases characterized by excessive osteoclast-mediated bone resorption.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Cre-Lox
SYK (spleen tyrosine kinase)
in vivo
mice
osteoclasts
tyrosine kinase
Megjelenés:Frontiers in Immunology. - 10 (2019), p. 937. -
További szerzők:Simon Edina (1981-) (ökológus) Alatshan, Ahmad (1984-) (immunológus) Aradi Petra Dobó Nagy Csaba (1961-) (fogszakorvos) Jakus Zoltán Benkő Szilvia (1973-) (molekuláris biológus) Győri Dávid Mócsai Attila
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM096580
035-os BibID:(cikkazonosító)2409 (WoS)000676356300001 (Scopus)85109904667
Első szerző:Kovács Elek Gergő
Cím:Caffeine Has Different Immunomodulatory Effect on the Cytokine Expression and NLRP3 Inflammasome Function in Various Human Macrophage Subpopulations / Elek Gergő Kovács, Ahmad Alatshan, Marietta Margit Budai, Zsolt Czimmerer, Eduárd Bíró, Szilvia Benkő
Dátum:2021
ISSN:2072-6643
Megjegyzések:Besides its well-known psychoactive effects, caffeine has a broad range of actions. It regulates several physiological mechanisms as well as modulates both native and adaptive immune responses by various ways. Although caffeine is assumed to be a negative regulator of inflammation, the effect on the secretion of pro- and anti-inflammatory cytokines is highly controversial. Macrophages are major mediators of inflammatory responses; however, the various subpopulations develop different effects ranging from the initiation to the resolution of inflammation. Here we report a comparative analysis of the effect of caffeine on two subpopulations of human monocyte-derived macrophages differentiated in the presence of macrophage colony-stimulating factor (M-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF), resulting in M-M?s and GM-M?s, respectively. We showed that although TNF-? secretion was downregulated in both LPS-activated M? subtypes by caffeine, the secretion of IL-8, IL-6, and IL-1? as well as the expression of Nod-like receptors was enhanced in M-M?s, while it did not change in GM-M?s. We showed that caffeine (1) altered adenosine receptor expression, (2) changed Akt/AMPK/mTOR signaling pathways, and (3) inhibited STAT1/IL-10 signaling axis in M-M?s. We hypothesized that these alterations play an important modulatory role in the upregulation of NLRP3 inflammasome-mediated IL-1? secretion in LPS-activated M-M?s following caffeine treatment.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
caffeine
inflammation
macrophages
NLRP3 inflammasome
cytokines
signaling
Megjelenés:Nutrients. - 13 : 7 (2021), p. 2409. -
További szerzők:Alatshan, Ahmad (1984-) (immunológus) Budai Marietta Margit (1985-) (molekuláris biológus) Czimmerer Zsolt (1981-) (molekuláris biológus) Bíró Eduárd (1998-) (molekuláris biológus) Benkő Szilvia (1973-) (molekuláris biológus)
Pályázati támogatás:K131844
OTKA
FK132185
OTKA
GINOP-2.3.2-15-2016-00040
GINOP
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM100844
035-os BibID:(cikkazonosító)e3001526 (WoS)000748720800001 (Scopus)85123845441 (PubMed)35085235
Első szerző:Tóth Krisztina
Cím:The NKCC1 ion transporter modulates microglial phenotype and inflammatory response to brain injury in a cell-autonomous manner / Tóth Krisztina, Lénárt Nikolett, Berki Péter, Fekete Rebeka, Szabadits Eszter, Pósfai Balázs, Cserép Csaba, Alatshan Ahmad, Benkő Szilvia, Kiss Dániel, Hübner Christian A., Gulyás Attila, Kaila Kai, Környei Zsuzsanna, Dénes Ádám
Dátum:2022
ISSN:1545-7885
Megjegyzések:The NKCC1 ion transporter contributes to the pathophysiology of common neurological disorders, but its function in microglia, the main inflammatory cells of the brain, has remained unclear to date. Therefore, we generated a novel transgenic mouse line in which microglial NKCC1 was deleted. We show that microglial NKCC1 shapes both baseline and reactive microglia morphology, process recruitment to the site of injury, and adaptation to changes in cellular volume in a cell-autonomous manner via regulating membrane conductance. In addition, microglial NKCC1 deficiency results in NLRP3 inflammasome priming and increased production of interleukin-1? (IL-1?), rendering microglia prone to exaggerated inflammatory responses. In line with this, central (intracortical) administration of the NKCC1 blocker, bumetanide, potentiated intracortical lipopolysaccharide (LPS)-induced cytokine levels. In contrast, systemic bumetanide application decreased inflammation in the brain. Microglial NKCC1 KO animals exposed to experimental stroke showed significantly increased brain injury, inflammation, cerebral edema and worse neurological outcome. Thus, NKCC1 emerges as an important player in controlling microglial ion homeostasis and inflammatory responses through which microglia modulate brain injury. The contribution of microglia to central NKCC1 actions is likely to be relevant for common neurological disorders.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Microglial cells
cytokines
Inflammation
Brain damage
Spleen
Edema
Intraperitoneal injections
Membrane potential
Megjelenés:PLOS Biology. - 20 : 1 (2022), p. e3001526. -
További szerzők:Lénárt Nikolett Berki Péter Fekete Rebeka Szabadits Eszter Pósfai Balázs Cserép Csaba Alatshan, Ahmad (1984-) (immunológus) Benkő Szilvia (1973-) (molekuláris biológus) Kiss Dániel Hübner, Christian A. Gulyás Attila Kaila, Kai Környei Zsuzsanna Dénes Ádám
Pályázati támogatás:LP2016-4/2016
MTA
ERC-CoG 724994
Egyéb
2019-2.1.7-ERA-NET-2020-00004
Egyéb
K131844
OTKA
BO/00558/19/5
MTA
ÚNKP-20-3-II
Egyéb
ÚNKP-21-5
Egyéb
SPP 1665 (German Research Foundation, DFG)
Egyéb
NEURON ACROBAT 01EW1706
Egyéb
Stipendium Hungaricum Scholarship
Egyéb
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Intézményi repozitóriumban (DEA) tárolt változat
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