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001-es BibID:	BIBFORM131144
035-os BibID:	(wos)001528019400001 (Scopus)105011040443
Első szerző:	Ahmad, Hala
Cím:	Retinoic acid differently modulates NOD1/NOD2-mediated inflammatory responses in human macrophage subsets / Ahmad Hala, Alatshan Ahmad, Bíró Eduárd, Benkő Szilvia
Dátum:	2025
ISSN:	1664-3224
Megjegyzések:	Macrophages are indispensable in homeostasis and innate immune responses in multiple tissues, while their polarization and functional characteristics are determined by the activating stimuli and their tissue microenvironment. The vitamin A derivative retinoic acid shows inhomogeneous distribution among the tissues and has an important modulatory role in inflammatory responses. However, its effects on the cytokine secretion induced by the cytosolic pattern-recognition receptors NOD1 and NOD2 are unclear. In our study, we used human monocyte-derived macrophages differentiated in the presence of GM-CSF or M-CSF to generate inflammation inducing (GM-M?) or inflammation resolving (M-M?) cells, respectively. We activated the cells with either a NOD1- or NOD2 specific agonist and, using ELISA, we determined the pattern and dynamics of cytokines secreted by the macrophage subpopulations. Furthermore, we studied the effect of all-trans retinoic acid (ATRA) pre-treatment on the NOD1- and NOD2-induced cytokine release. Our comparative analysis shows subpopulation-characteristic pattern of cytokine secretion, as GM-M? produce significantly higher pro-inflammatory IL-6, IL-8, TNF-? and IL-1?, while M-M? secret higher anti-inflammatory IL-10. However, IL-18 and IFN? secretion was comparable between the M? subpopulations. We also show for the first time that ATRA has marked impact on cytokine secretion triggered by NOD1 and NOD2. Importantly however, the ATRA-induced changes of cytokine secretion follow opposite tendency in two M? subpopulations. In conclusion, these results show that NOD1/NOD2-induced cytokine secretion by macrophage subsets is highly context-dependent and our results highlight the importance of the retinoic acid content of the local tissue environment in shaping macrophage function in health and disease.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk retinoic acid NOD1 NOD2 NOD-like receptor vitamin A inflammation macrophage cytokine
Megjelenés:	Frontiers in Immunology. - 16 (2025), p. 1-11. -
További szerzők:	Alatshan, Ahmad (1984-) (immunológus) Bíró Eduárd (1998-) (molekuláris biológus) Benkő Szilvia (1973-) (molekuláris biológus)
Pályázati támogatás:	K131844 OTKA K147109 OTKA Richter Talentum Foundation Egyéb Stipendium Hungaricum Scholarship Egyéb
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001-es BibID:	BIBFORM128580
035-os BibID:	(Scopus)86000334207 (WoS)001438314000001
Első szerző:	Fekete Réka (biológus)
Cím:	Microglia dysfunction, neurovascular inflammation and focal neuropathologies are linked to IL-1- and IL-6-related systemic inflammation in COVID-19 / Fekete Rebeka, Simats Alba, Bíró Eduárd, Pósfai Balázs, Cserép Csaba, Schwarcz Anett D., Szabadits Eszter, Környei Zsuzsanna, Tóth Krisztina, Fichó Erzsébet, Szalma János, Vida Sára, Kellermayer Anna, Dávid Csaba, Acsády László, Kontra Levente, Silvestre-Roig Carlos, Moldvay Judit, Fillinger János, Csikász-Nagy Attila, Hortobágyi Tibor, Liesz Arthur, Benkő Szilvia, Dénes Ádám
Dátum:	2025
ISSN:	1097-6256 1546-1726
Megjegyzések:	COVID-19 is associated with diverse neurological abnormalities, but the underlying mechanisms are unclear. We hypothesized that microglia, the resident immune cells of the brain, are centrally involved in this process. To study this, we developed an autopsy platform allowing the integration of molecular anatomy, protein and mRNA datasets in postmortem mirror blocks of brain and peripheral organ samples from cases of COVID-19. We observed focal loss of microglial P2Y12R, CX3CR1?CX3CL1 axis deficits and metabolic failure at sites of virus-associated vascular inflammation in severely affected medullary autonomic nuclei and other brain areas. Microglial dysfunction is linked to mitochondrial injury at sites of excessive synapse and myelin phagocytosis and loss of glutamatergic terminals, in line with proteomic changes of synapse assembly, metabolism and neuronal injury. Furthermore, regionally heterogeneous microglial changes are associated with viral load and central and systemic inflammation related to interleukin (IL)-1 or IL-6 via virus-sensing pattern recognition receptors and inflammasomes. Thus, SARS-CoV-2-induced inflammation might lead to a primarily gliovascular failure in the brain, which could be a common contributor to diverse COVID-19-related neuropathologies.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Diseases of the nervous system Neuroimmunology
Megjelenés:	Nature Neuroscience. - 28 : 3 (2025), p. 558-576. -
További szerzők:	Simats, Alba Bíró Eduárd (1998-) (molekuláris biológus) Pósfai Balázs Cserép Csaba Schwarcz, Anett D. Szabadits Eszter Környei Zsuzsanna Tóth Krisztina Fichó Erzsébet Szalma János Vida Sára Kellermayer Anna Dávid Csaba Acsády László Kontra Levente Silvestre-Roig, Carlos Moldvay Judit Fillinger János Csikász-Nagy Attila Hortobágyi Tibor G. (1998-) (orvostanhallgató) Liesz, Arthur Benkő Szilvia (1973-) (molekuláris biológus) Dénes Ádám
Pályázati támogatás:	K 131844 OTKA ÚNKP-23-5 Egyéb ÚNKP-23-4-I Egyéb NKFIH SNN132999 Egyéb ÚNKP-22-3 Egyéb K 147109 OTKA
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001-es BibID:	BIBFORM092036
035-os BibID:	(scopus)85099982357 (wos)000615305700001
Első szerző:	Fekete Tünde (immunológus, molekuláris biológus, mikrobiológus)
Cím:	Focusing on the Cell Type Specific Regulatory Actions of NLRX1 / Tünde Fekete, Dóra Bencze, Eduárd Bíró, Szilvia Benkő, Kitti Pázmándi
Dátum:	2021
ISSN:	1661-6596 1422-0067
Megjegyzések:	Cells utilize a diverse repertoire of cell surface and intracellular receptors to detect exogenous or endogenous danger signals and even the changes of their microenvironment. However, some cytosolic NOD-like receptors (NLR), including NLRX1, serve more functions than just being general pattern recognition receptors. The dynamic translocation between the cytosol and the mitochondria allows NLRX1 to interact with many molecules and thereby to control multiple cellular functions. As a regulatory NLR, NLRX1 fine-tunes inflammatory signaling cascades, regulates mitochondriaassociated functions, and controls metabolism, autophagy and cell death. Nevertheless, literature data are inconsistent and often contradictory regarding its effects on individual cellular functions. One plausible explanation might be that the regulatory effects of NLRX1 are highly cell type specific and the features of NLRX1 mediated regulation might be determined by the unique functional activity or metabolic profile of the given cell type. Here we review the cell type specific actions of NLRX1 with a special focus on cells of the immune system. NLRX1 has already emerged as a potential therapeutic target in numerous immune-related diseases, thus we aim to highlight which regulatory properties of NLRX1 are manifested in disease-associated dominant immune cells that presumably offer promising therapeutic solutions to treat these disorders.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	International Journal of Molecular Sciences. - 22 : 3 (2021), p. 1316. -
További szerzők:	Bencze Dóra (1992-) Bíró Eduárd (1998-) (molekuláris biológus) Benkő Szilvia (1973-) (molekuláris biológus) Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus)
Pályázati támogatás:	OTKA-131844 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM096580
035-os BibID:	(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
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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