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1.

001-es BibID:BIBFORM101339
035-os BibID:(cikkazonosító)4140 (scopus)85127787477 (wos)000786332700001
Első szerző:Ádám Dorottya (molekuláris biológus)
Cím:Opioidergic Signaling : a Neglected, Yet Potentially Important Player in Atopic Dermatitis / Dorottya Ádám, József Arany, Kinga Fanni Tóth, Balázs István Tóth, Attila Gábor Szöllősi, Attila Oláh
Dátum:2022
ISSN:1661-6596 1422-0067
Megjegyzések:Atopic dermatitis (AD) is one of the most common skin diseases, the prevalence of which is es-pecially high among children. Although our understanding about its pathogenesis has substan-tially grown in recent years, and hence, several novel therapeutic targets have been successfully exploited in the management of the disease, we still lack curative treatments for it. Thus, there is an unmet societal demand to identify further details of its pathogenesis to thereby pave the way for novel therapeutic approaches with favorable side effect profiles. It is commonly accepted that dysfunction of the complex cutaneous barrier plays a central role in the development of AD; therefore, the signaling pathways involved in the regulation of this quite complex process are likely to be involved in the pathogenesis of the disease and can provide novel, promising, yet unexplored therapeutic targets. Thus, in the current review, we aim to summarize the available potentially AD-relevant data regarding one such signaling pathway, namely cutaneous opi-oidergic signaling.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
atopic dermatitis (AD)
cutaneous barrier
[delta]-opioid receptor (DOR)
inflammation
itch
[delta]-opioid receptor (KOR)
keratinocyte
mast cell
[delta]-opioid receptor (MOR)
nociceptin/orphanin FQ (NOP) receptor
opioid
skin
Megjelenés:International Journal Of Molecular Sciences. - 23 : 8 (2022), p. 4140. -
További szerzők:Arany József (1990-) (klinikai laboratóriumi kutató, vegyész) Tóth Kinga Fanni (1992-) (molekuláris biológus, élettanász) Tóth István Balázs (1978-) (élettanász) Szöllősi Attila Gábor (1982-) (élettanász) Oláh Attila (1984-) (élettanász)
Pályázati támogatás:GINOP-2.3.2-15-2016-00026
GINOP
NKFIH 120187
Egyéb
NKFIH 134235
Egyéb
NKFIH 134725
Egyéb
NKFIH 134993
Egyéb
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
Bolyai János Kutatási Ösztöndíj (BO/00660/21/5)
MTA
Bolyai János Kutatási Ösztöndíj (BO/00905/19/5)
MTA
ÚNKP-21-5-DE-465
Egyéb
ÚNKP-21-5-DE-491
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

2.

001-es BibID:BIBFORM106381
035-os BibID:(PMID)36502939 (WoS)000984536200001 (Scopus)85149686723
Első szerző:Alimohammadi, Shahrzad (Gyógyszerész)
Cím:TRPV4 activation increases the expression of CD207 (Langerin) of monocyte-derived Langerhans cells, without affecting their maturation / Alimohammadi Shahrzad, Pénzes Zsófia, Horváth Dorottya, Gyetvai Ágnes, Bácsi Attila, Kis Nikoletta Gréta, Németh Ákos, Arany József, Oláh Attila, Lisztes Erika, Tóth Balázs István, Bíró Tamás, Szöllősi Attila Gábor
Dátum:2023
ISSN:0022-202X 1523-1747
Megjegyzések:Langerhans cells (LCs) are the sole professional antigen-presenting cell normally found in the human epidermal compartment. Research into their physiological role is hindered by the fact that they are invariably activated during isolation from the skin. To overcome this challenge, we turned to a monocyte-derived LC model (moLC), which we characterized with RNASeq, and compared the transcriptome of moLCs to donor-matched immature dendritic cells. We found that moLCs express markers characteristic of LC2 cells, as well as transient receptor potential vanilloid 4 (TRPV4). TRPV4 is especially important in skin, as it has been linked to conservation of the skin barrier, immunological responses as well as acute and chronic itch, but we know little about its function on LCs. Our results show that TRPV4 activation increased the expression of Langerin and led to increased intracellular calcium concentration in moLCs. Regarding the functionality of moLCs, we found that TRPV4 agonism had a mitigating effect on their inflammatory responses, since it decreased their cytokine production, and T cell activating capability. As TRPV4 has emerged as a potential therapeutic target in dermatological conditions, it is important to highlight LCs as a novel target of these therapies.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Langerhans sejt
Dendritikus sejt
Immunológia
Természetes immunitás
Megjelenés:Journal Of Investigative Dermatology. - 143 : 5 (2023), p. 801-811.e10. -
További szerzők:Pénzes Zsófia (1992-) (klinikai laboratóriumi kutató) Horváth Dorottya (1994-) (molekuláris biológus) Gyetvai Ágnes Bácsi Attila (1967-) (immunológus) Kis Gréta (1979-) (környezetkutató) Németh Ákos (1984-) (gyógyszer-vegyészmérnök, közgazdász) Arany József (1990-) (klinikai laboratóriumi kutató, vegyész) Oláh Attila (1984-) (élettanász) Lisztes Erika (1986-) (élettanász) Tóth István Balázs (1978-) (élettanász) Bíró Tamás (1968-) (élettanász) Szöllősi Attila Gábor (1982-) (élettanász)
Pályázati támogatás:125053
OTKA
128034
OTKA
134235
OTKA
GINOP-2.3.2-15-2016-00015
GINOP
GINOP-2.3.3-15-2016-00020
GINOP
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
MTA-DE
MTA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

001-es BibID:BIBFORM116427
Első szerző:Tóth Kinga Fanni (molekuláris biológus, élettanász)
Cím:Fluoxetine exerts anti-inflammatory effects on human epidermal keratinocytes, and suppresses their endothelin release / Tóth K. F., Ádám D., Arany J., Ramirez Y. A., Bíró T., Drake J. I., O'Mahony A., Szöllősi A. G., Kilic A., Soeberdt M., Abels C., Oláh A.
Dátum:2023
ISSN:0022-202X 1523-1747
Megjegyzések:Pathological activity Toll-like receptor (TLR)-3 plays an important role in the pathogenesis of pruritic dermatoses and in the development of itch. Fluoxetine is a safe antidepressant with remarkable anti-inflammatory actions in various systems, including the skin. Thus, we aimed to investigate the effects of fluoxetine in a TLR3-activator induced inflammatory model by using immortalized (HaCaT) as well as primary human epidermal keratinocytes. When applied at a non-cytotoxic concentration (MTT-assay, CyQUANT-assay), fluoxetine significantly suppressed polyinosinic-polycytidylic acid (p(I:C))-induced expression and release of several proinflammatory cytokines, and it decreased the release of the itch mediator endothelins (Q-PCR, cytokine array, ELISA). Fluoxetine did not interfere with the p(I:C)-induced activation of the p38 MAPK cascade, and did not inhibit phosphorylation (and hence inactivation) of IkBa, an important inhibitor of the NF-kB pathway (western blot). Moreover, co-administration of fluoxetine failed to significantly suppress p(I:C)-induced elevation ofmitochondrial ROS production (MitoSOX Red). Instead, the anti-inflammatory effects of fluoxetine were most likely mediated via the inhibition of the phosphoinositide 3-kinase (PI3K)-pathway (unbiased activity profiling). Importantly, the PI3K-inhibitor GDC0941 fully mimicked the effects of fluoxetine. Although fluoxetine was found to be able to occupy the binding site of GDC0941 (in silico molecular docking), and to exert direct inhibitory effect on PI3K, it exhibited much lower potency and efficacy as compared to GDC0941 (cell-free PI3K activity assay). Collectively, our findings demonstrate that fluoxetine exerts potent anti-inflammatory effects, and suppresses the release of the endogenous itch mediator endothelins in human keratinocytes, most likely via indirect inhibition of PI3K. Thus, clinical studies are encouraged to explore whether the currently reported beneficial effects translate in vivo following its topical administration in inflammatory and pruritic dermatoses. Supported by: NRDIO (125055, 134235, 134993, GINOP-2.3.2-15-2016-00015, GINOP-2.3.3-15-2016-00020, EFOP-3.6.3-VEKOP-16-2017-00009); János Bolyai Research Scholarship; ÚNKP-23-5-DE-477; "Deutscher Akademischer Austauschdienst" (DAAD); Dr. AugustWolff GmbH & Co. KG Arzneimittel.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
fluoxetine
itch
inflammation
skin
keratinocyte
endothelin
Toll-like receptor 3
Megjelenés:Journal Of Investigative Dermatology. - 143 : 11 (2023), p. S361. -
További szerzők:Ádám Dorottya (1991-) (molekuláris biológus) Arany József (1990-) (klinikai laboratóriumi kutató, vegyész) Ramirez, Yesid A. Bíró Tamás (1968-) (élettanász) (absztraktok) Drake, Jennifer I. O'Mahony, Alison Szöllősi Attila Gábor (1982-) (élettanász) Kilic, Ana Soeberdt, Michael Abels, Christoph Oláh Attila (1984-) (élettanász)
Pályázati támogatás:125055
OTKA
134235
OTKA
134993
OTKA
GINOP-2.3.2-15-2016-00015
GINOP
GINOP-2.3.3-15-2016-00020
GINOP
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
János Bolyai Research Scholarship
MTA
ÚNKP-23-5-DE-477
Egyéb
Deutscher Akademischer Austauschdienst
Egyéb
Dr. AugustWolff GmbH & Co. KG Arzneimittel
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

001-es BibID:BIBFORM116512
035-os BibID:(Scopus)85180437359 (cikkazonosító)e14988 (WoS)001128766100001
Első szerző:Tóth Kinga Fanni (molekuláris biológus, élettanász)
Cím:Fluoxetine exerts anti-inflammatory effects on human epidermal keratinocytes and suppresses their endothelin release / Tóth Kinga Fanni, Ádám Dorottya, Arany József, Ramirez Yesid A., Bíró Tamás, Jennifer I. Drake, Alison O'Mahony, Szöllősi Attila Gábor, Póliska Szilárd, Ana Kilic, Michael Soeberdt, Christoph Abels, Oláh Attila
Dátum:2024
ISSN:0906-6705
Megjegyzések:Fluoxetine is a safe antidepressant with remarkable anti-inflammatory actions; therefore, we aimed to investigate its effects on immortalized (HaCaT) as well as primary human epidermal keratinocytes in a polyinosinic-polycytidylic acid (p(I:C))-induced inflammatory model. We found that a non-cytotoxic concentration (MTT-assay, CyQUANT-assay) of fluoxetine significantly suppressed p(I:C)-induced expression and release of several pro-inflammatory cytokines (Q-PCR, cytokine array, ELISA), and it decreased the release of the itch mediator endothelins (ELISA). These effects were not mediated by the inhibition of the NF-?B or p38 MAPK pathways (western blot), or by the suppression of the p(I:C)-induced elevation of mitochondrial ROS production (MitoSOX Red labeling). Instead, unbiased activity profiling revealed that they were most likely mediated via the inhibition of the phosphoinositide 3-kinase (PI3K) pathway. Importantly, the PI3K-inhibitor GDC0941 fully mimicked the effects of fluoxetine (Q-PCR, ELISA). Although fluoxetine was able to occupy the binding site of GDC0941 (in silico molecular docking), and exerted direct inhibitory effect on PI3K (cell-free PI3K activity assay), it exhibited much lower potency and efficacy as compared to GDC0941. Finally, RNA-Seq analysis revealed that fluoxetine deeply influenced the transcriptional alterations induced by p(I:C)-treatment, and exerted an overall anti-inflammatory activity. Collectively, our findings demonstrate that fluoxetine exerts potent anti-inflammatory effects, and suppresses the release of the endogenous itch mediator endothelins in human keratinocytes, most likely via interfering with the PI3K pathway. Thus, clinical studies are encouraged to explore whether the currently reported beneficial effects translate in vivo following its topical administration in inflammatory and pruritic dermatoses.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
atopic dermatitis
fluoxetine
PI3K
Toll-like receptor 3
inflammation
keratinocyte
itch
endothelin
Megjelenés:Experimental Dermatology. - 33 : 1 (2024), p. 1-15. -
További szerzők:Ádám Dorottya (1991-) (molekuláris biológus) Arany József (1990-) (klinikai laboratóriumi kutató, vegyész) Ramirez, Yesid A. Bíró Tamás (1968-) (élettanász) Drake, Jennifer I. O'Mahony, Alison Szöllősi Attila Gábor (1982-) (élettanász) Póliska Szilárd (1978-) (biológus) Kilic, Ana Soeberdt, Michael Abels, Christoph Oláh Attila (1984-) (élettanász)
Pályázati támogatás:GINOP-2.3.2-15-2016-00015
GINOP
GINOP-2.3.3-15-2016-00020
GINOP
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
NKFIH 125055
Egyéb
NKFIH 134235
Egyéb
NKFIH 134993
Egyéb
János Bolyai Research Scholarship
MTA
ÚNKP-22-5-DE-427
Egyéb
ÚNKP-23-5-DE-477
Egyéb
TKP2021-NKTA-34
Egyéb
Deutscher Akademischer Austauschdienst
Egyéb
Dr. August Wolff GmbH & Co. KG Arzneimittel
Egyéb
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

5.

001-es BibID:BIBFORM115844
Első szerző:Tóth Kinga Fanni (molekuláris biológus, élettanász)
Cím:Fluoxetine exerts anti-inflammatory effects on human epidermal keratinocytes, and suppresses endothelin release via inhibiting PI3K / Tóth K., Ádám D., Arany J., Ramirez Y. A., Bíró T., Drake J. I., O'Mahony A., Szöllösi A. G., Kilic A., Soeberdt M., Abels C., Oláh A.
Dátum:2023
ISSN:0022-202X 1523-1747
Megjegyzések:Fluoxetine (FX) is a safe antidepressant belonging to the group of selective serotonin reuptake inhibitors. It exhibits remarkable anti-inflammatory activity in various systems; thus, we aimed to investigate its biological effects on immortalized (HaCaT) and primary human epidermal keratinocytes. We found that, when applied at its highest non-cytotoxic concentration (14 mM), FX significantly suppressed the Toll-like receptor 3 activator polyinosinicpolycytidylic acid (p(I:C))-induced expression (Q-PCR: interleukin [IL]-1a, IL-1b, and IL-8) and release (cytokine array and ELISA: IL-8) of several pro-inflammatory cytokines, and it decreased the release of the itch mediator endothelins as well. Surprisingly, unbiased activity profiling revealed that the effects of FX (4.7 and 14 mM) did not resemble the effects of different doses of serotonin, but were rather similar to the effects of the phosphoinositide 3-kinase (PI3K) inhibitor GDC0941 (370 nM). In addition, GDC0941 mimicked the effects of FX in our experimental models, and in silico docking analysis revealed that FX may be able to occupy the same binding site on PI3K isoenzymes as GDC0941. Finally, we found that FX was indeed able to directly suppress activity of PI3K (cell-free PI3K activity assay). Collectively, our findings demonstrate that FX (14 mM) exerts potent anti-inflammatory effects, and suppresses the release of the endogenous itch mediator endothelins in human keratinocytes, most likely via the inhibition of PI3K. Thus, our data highlight the possibility of dermatological repositioning of FX to treat various inflammatory and pruritic dermatoses.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
fluoxetine
keratinocyte
itch
inflammation
Megjelenés:Journal Of Investigative Dermatology. - 143 : 5 (2023), p. S126. -
További szerzők:Ádám Dorottya (1991-) (molekuláris biológus) Arany József (1990-) (klinikai laboratóriumi kutató, vegyész) Ramirez, Yesid A. Bíró Tamás (1968-) (élettanász) (absztraktok) Drake, Jennifer I. O'Mahony, Alison Szöllősi Attila Gábor (1982-) (élettanász) Kilic, Ana Soeberdt, Michael Abels, Christoph Oláh Attila (1984-) (élettanász)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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