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001-es BibID:	BIBFORM001015
Első szerző:	Bíró Tamás (élettanász)
Cím:	TRP channels as novel players in the pathogenesis and therapy of itch / Tamás Bíró, Balázs I. Tóth, Rita Marincsák, Nóra Dobrosi, Tamás Géczy, Ralf Paus
Dátum:	2007
ISSN:	0925-4439
Megjegyzések:	Itch (pruritus) is a sensory phenomenon characterized by a (usually) negative affective component and the initiation of a special behavioral act, i.e. scratching. Older studies predominantly have interpreted itch as a type of pain. Recent neurophysiological findings, however, have provided compelling evidence that itch (although it indeed has intimate connections to pain) rather needs to be understood as a separate sensory modality. Therefore, a novel pruriceptive system has been proposed, within which itch-inducing peripheral mediators (pruritogens), itch-selective receptors (pruriceptors), sensory afferents and spinal cord neurons, and defined, itch-processing central nervous system regions display complex, layered responses to itch. In this review, we begin with a current overview on the neurophysiology of pruritus, and distinguish it from that of pain. We then focus on the functional characteristics of the large family of transient receptor potential (TRP) channels in skin-coupled sensory mechanisms, including itch and pain. In particular, we argue that - due to their expression patterns, activation mechanisms, regulatory roles, and pharmacological sensitivities - certain thermosensitive TRP channels are key players in pruritus pathogenesis. We close by proposing a novel, TRP-centered concept of pruritus pathogenesis and sketch important future experimental directions towards the therapeutic targeting of TRP channels in the clinical management of itch.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban TRP channels pruritogens pruriceptive itch
Megjelenés:	Biochimica et Biophysica Acta (BBA). Molecular Basis of Disease. - 1772 : 8 (2007), p. 1004-1021. -
További szerzők:	Tóth István Balázs (1978-) (élettanász) Marincsák Rita (1979-) (fogszakorvos) Dobrosi Nóra (1981-) (molekuláris biológus) Géczy Tamás (1980-) (élettanász) Paus, Ralf
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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001-es BibID:	BIBFORM078435
035-os BibID:	(PMID)30389578
Első szerző:	Nyakundi, Benard Bogonko (biokémikus)
Cím:	Oxidized hemoglobin forms contribute to NLRP3 inflammasome-driven IL1[beta] production upon intravascular hemolysis / Benard Bogonko Nyakundi, Andrea Tóth, Enikő Balogh, Béla Nagy, Judit Erdei, Bernhard Ryffel, György Paragh, Mario D. Cordero, Viktória Jeney
Dátum:	2019
Megjegyzések:	Damage associated molecular patterns (DAMPs) are released form red blood cells (RBCs) during intravascular hemolysis (IVH). Extracellular heme, with its pro-oxidant, pro-inflammatory and cytotoxic effects, is sensed by innate immune cells through pattern recognition receptors such as toll-like receptor 4 and nucleotide-binding domain and leucine rich repeat containing family, pyrin domain containing 3 (NLRP3), while free availability of heme is strictly controlled. Here we investigated the involvement of different hemoglobin (Hb) forms in hemolysis-associated inflammatory responses. We found that after IVH most of the extracellular heme molecules are localized in oxidized Hb forms. IVH was associated with caspase-1 activation and formation of mature IL-1β in plasma and in the liver of C57BL/6 mice. We showed that ferrylHb (FHb) induces active IL-1β production in LPS-primed macrophages in vitro and triggered intraperitoneal recruitment of neutrophils and monocytes, caspase-1 activation and active IL-1β formation in the liver of C57BL/6 mice. NLRP3 deficiency provided a survival advantage upon IVH, without influencing the extent of RBC lysis or the accumulation of oxidized Hb forms. However, both hemolysis-induced and FHb-induced pro-inflammatory responses were largely attenuated in Nlrp3-/- mice. Taken together, FHb is a potent trigger of NLRP3 activation and production of IL-1β in vitro and in vivo, suggesting that FHb may contribute to hemolysis-induced inflammation. Identification of RBC-derived DAMPs might allow us to develop new therapeutic approaches for hemolytic diseases.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Ferryl hemoglobin Heme Hemolysis IL-1β Macrophage NLRP3 inflammasome activation
Megjelenés:	Biochimica et biophysica acta. Molecular basis of disease. - 1865 : 2 (2019), p. 464-475. -
További szerzők:	Tóth Andrea (1992-) (molekuláris biológus) Balogh Enikő (1987-) (molekuláris biológus) Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos) Erdei Judit Zsuzsa (1992-) (vegyész) Ryffel, Bernhard Paragh György (1953-) (belgyógyász) Cordero, Mario D. Jeney Viktória (1971-) (vegyész, kémia tanár)
Pályázati támogatás:	NKFIH K116024 NKFIH GINOP-2.3.2-15-2016-00005 GINOP
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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