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001-es BibID:	BIBFORM100838
035-os BibID:	(cikkazonosító)745658 (scopus)85127275074 (wos)000773609500001
Első szerző:	Szöllősi Attila Gábor (élettanász)
Cím:	Pruritus : Sensory Symptom Generated in Cutaneous Immuno-Neuronal Crosstalk / Szöllősi Attila Gábor, Oláh Attila, Lisztes Erika, Griger Zoltán, Tóth Balázs István
Dátum:	2022
ISSN:	1663-9812
Megjegyzések:	Pruritus or itch generated in the skin is one of the most widespread symptoms associated with various dermatological and systemic (immunological) conditions. Although many details about the molecular mechanisms of the development of both acute and chronic itch were uncovered in the last 2 decades, our understanding is still incomplete and the clinical management of pruritic conditions is one of the biggest challenges in daily dermatological practice. Recent research revealed molecular interactions between pruriceptive sensory neurons and surrounding cutaneous cell types including keratinocytes, as well as resident and transient cells of innate and adaptive immunity. Especially in inflammatory conditions, these cutaneous cells can produce various mediators, which can contribute to the excitation of pruriceptive sensory fibers resulting in itch sensation. There also exists significant communication in the opposite direction: sensory neurons can release mediators that maintain an inflamed, pruritic tissue-environment. In this review, we summarize the current knowledge about the sensory transduction of pruritus detailing the local intercellular interactions that generate itch. We especially emphasize the role of various pruritic mediators in the bidirectional crosstalk between cutaneous non-neuronal cells and sensory fibers. We also list various dermatoses and immunological conditions associated with itch, and discuss the potential immune-neuronal interactions promoting the development of pruritus in the particular diseases. These data may unveil putative new targets for antipruritic pharmacological interventions.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk itch molecular transduction of pruritus sensory neurons inflammation skin cytokines dermatoses
Megjelenés:	Frontiers in Pharmacology. - 13 (2022), p. 745658. -
További szerzők:	Oláh Attila (1984-) (élettanász) Lisztes Erika (1986-) (élettanász) Griger Zoltán (1979-) (belgyógyász, allergológus és klinikai immunológus, reumatológus) Tóth István Balázs (1978-) (élettanász)
Pályázati támogatás:	NKFIH 120187 Egyéb NKFIH 134235 Egyéb NKFIH 134725 Egyéb NKFIH 134791 Egyéb NKFIH 134993 Egyéb EFOP-3.6.3-VEKOP-16-2017-00009 EFOP GINOP-2.3.2-15-2016-00050 GINOP ÚNKP-20-5-DE-100 Egyéb ÚNKP-21-5-DE-465 Egyéb ÚNKP-21-5-DE-491 Egyéb
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001-es BibID:	BIBFORM111641
035-os BibID:	(scopus)85160027968 (cikkazonosító)1168359
Első szerző:	Vincze Anett
Cím:	Pruritogenic molecules in the skin of patients with dermatomyositis / Vincze Anett, Herczeg-Lisztes Erika, Szabó Katalin, Béldi Tibor Gábor, Nagy-Vincze Melinda, Pór Ágnes, Varga József, Dankó Katalin, Biró Tamás, Tóth Balázs István, Griger Zoltán
Dátum:	2023
ISSN:	2296-858X
Megjegyzések:	Introduction: Pruritus is a common excruciating symptom in systemic autoimmune diseases such as dermatomyositis (DM) but the pathogenesis is not fully understood. We intended to investigate the targeted expression analysis of candidate molecules involved in the development of pruritus in lesional vs. non-lesional skin samples of patients affected with active DM. We looked for correlations between the investigated pruriceptive signaling molecules, disease activity, and itching sensation of DM patients. Methods: Interleukins (IL-33 and IL-6), tumor necrosis factor ? (TNF-?), peroxisome proliferator-activated receptor ? (PPAR-?), and ion channels belonging to the transient receptor potential (TRP) family were analyzed. The expression of TNF-?, PPAR-?, IL-33, IL-6, and TRP channels in lesional DM skin was evaluated by RT-qPCR and immunohistochemistry and was compared with non-lesional DM skin samples. Pruritus, disease activity, and damage of DM were evaluated by the 5-D itch scale and Cutaneous Dermatomyositis Disease Area and Severity Index (CDASI), respectively. Statistical analysis was performed with IBM SPSS 28 software. Results: A total of 17 active DM patients participated in the study. We could show that the itching score was positively correlated with the CDASI activity score (Kendall's tau-b = 0.571; p = 0.003). TNF-? gene expression was significantly higher in lesional DM skin than in non-lesional DM skin (p = 0.009) and differed in the subgroups of patients with different itch intensities (p = 0.038). The mRNA expression of lesional IL-6 correlated positively with 5-D itch and CDASI activity score (Kendall's tau-b = 0.585; p = 0.008 and 0.45; p = 0.013, respectively). TRPV4 expressions were positively correlated with CDASI damage score (Kendall's tau-b = 0.626; p < 0.001), but the mRNA expressions of the TRP family, PPAR-?, IL-6, and IL-33 were not different in lesional and non-lesional samples. Immunohistochemistry analysis did not find significant alterations in the expressions of TNF-?, PPAR-?, IL-6, and IL-33 in lesional and non-lesional regions. Discussion: Our results argue that cutaneous disease activity, TNF-?, and IL-6 might play a central role in DM-associated itch, while TRPV4 plays a central role in tissue regeneration.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk dermatomyositis inflammatory myopathies itch pruritus TRP channels TNF-α IL-6
Megjelenés:	Frontiers in Medicine. - 10 (2023), p. 1168359. -
További szerzők:	Lisztes Erika (1986-) (élettanász) Szabó Katalin (1991-) (orvos) Béldi Tibor (1994-) (orvos) Nagy-Vincze Melinda (1985-) (orvos) Pór Ágnes Varga József (1955-) (fizikus) Dankó Katalin (1952-2021) (belgyógyász, allergológus és klinikai immunológus) Bíró Tamás (1968-) (élettanász) Tóth István Balázs (1978-) (élettanász) Griger Zoltán (1979-) (belgyógyász, allergológus és klinikai immunológus, reumatológus)
Pályázati támogatás:	134791 OTKA 120187 OTKA EFOP-3.6.3-VEKOP-16-2017-00009 EFOP Bolyai János Kutatási Ösztöndíj Egyéb
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