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001-es BibID:	BIBFORM078224
Első szerző:	Póliska Szilárd (biológus)
Cím:	Gene expression analysis of vascular pathophysiology related to anti-TNF treatment in rheumatoid arthritis / Szilárd Póliska, Timea Besenyei, Edit Végh, Attila Hamar, Anita Pusztai, Andrea Váncsa, Nóra Bodnár, Szilvia Szamosi, Mária Csumita, György Kerekes, Zoltán Szabó, Zoltán Nagy, Gabriella Szűcs, Sándor Szántó, Gábor Zahuczky, László Nagy, Zoltán Szekanecz
Dátum:	2019
ISSN:	1478-6354 1478-6362
Megjegyzések:	Objectives: Impaired vascular pathophysiology and increased cardiovascular (CV) mortality are associated with rheumatoid arthritis (RA). To date, no genomic analysis of RA- and RA treatment-related vascular pathophysiology has been published. In this pilot study, we performed gene expression profiling in association with vascular pathophysiology in RA patients. Methods: Sixteen and 19 biologic-naïve RA patients were included in study 1 and study 2, respectively. In study 1, genetic signatures determined by microarray were related to flow-mediated vasodilation (FMD), pulse-wave velocity (PWV), and common carotid intima-media thickness (IMT) of patients. In study 2, clinical response (cR) vs non-response (cNR) to 1-year etanercept (ETN) or certolizumab pegol (CZP) treatment, as well as "vascular" response (vR) vs non-response (vNR) to biologics, were also associated with genomic profiles. Multiple testing could not be performed due to the relatively small number of patients; therefore, our pilot study may lack power. Results: In study 1, multiple genes were up- or downregulated in patients with abnormal vs normal FMD, IMT, and PWV. In study 2, there were 13 cR and 6 cNR anti-tumor necrosis factor (TNF)-treated patients. In addition, 10, 9, and 8 patients were FMD-20%, IMT-20%, and PWV-20% responders. Again, vascular responder status was associated with changes of the expression of various genes. The highest number of genes showing significant enrichment were involved in positive regulation of immune effector process, regulation of glucose transport, and Golgi vesicle budding. Conclusion: Differential expression of multiple genetic profiles may be associated with vascular pathophysiology associated with RA. Moreover, distinct genetic signatures may also be associated with clinical and vascular responses to 1-year anti-TNF treatment.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Arthritis Research & Therapy. - 21 : 1 (2019), p. 94. -
További szerzők:	Besenyei Tímea (1980-) (reumatológus, belgyógyász) Végh Edit (1978-) (reumatológus, belgyógyász) Hamar Attila Béla (1990-) (általános orvos) Karancsiné Pusztai Anita (1989-) (tudományos segédmunkatárs) Váncsa Andrea (1972-) (orvos) Bodnár Nóra (1980-) (reumatológus) Szamosi Szilvia (1975-) (belgyógyász, reumatológus) Csumita Mária (1989-) (biomérnök) Kerekes György (1973-) (belgyógyász, kardiológus, angiológus) Szabó Zoltán (1970-) (belgyógyász, reumatológus) Nagy Zoltán (orvos) Szűcs Gabriella (1963-) (belgyógyász, allergológus és klinikai immunológus, reumatológus) Szántó Sándor (1968-) (belgyógyász, reumatológus) Zahuczky Gábor (1975-) (molekuláris biológus, biokémikus, vegyész) Nagy László (1966-) (molekuláris sejtbiológus, biokémikus) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus)
Pályázati támogatás:	K10073 OTKA TAMOP-4.2.4.A/2-11/1-2012-0001 TÁMOP GINOP-2.3.2-15-2016-00015 GINOP GINOP-2.3.2-15-2016-00050 GINOP
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM007092
Első szerző:	Szántó Sándor (belgyógyász, reumatológus)
Cím:	Inhibition of indoleamine 2,3-dioxygenase-mediated tryptophan catabolism accelerates collagen-induced arthritis in mice / Szanto, S., Koreny, T., Mikecz, K., Glant, T. T., Szekanecz, Z., Varga, J.
Dátum:	2007
ISSN:	1478-6362 (Electronic)
Megjegyzések:	Indoleamine 2,3-dioxygenase (IDO) is one of the initial and rate-limiting enzymes involved in the catabolism of the essential amino acid tryptophan. In cultured cells, the induction of IDO leads to depletion of tryptophan and tryptophan starvation. Recent studies suggest that modulation of tryptophan concentration via IDO plays a fundamental role in innate immune responses. Induction of IDO by interferon-gamma in macrophages and dendritic cells results in tryptophan depletion and suppresses the immune-mediated activation of fibroblasts and T, B, and natural killer cells. To assess the role of IDO in collagen-induced arthritis (CIA), a model of rheumatoid arthritis characterized by a primarily Th1-like immune response, activity of IDO was inhibited by 1-methyl-tryptophan (1-MT) in vivo. The results showed significantly increased incidence and severity of CIA in mice treated with 1-MT. Activity of IDO, as determined by measuring the levels of kynurenine/tryptophan ratio in the sera, was increased in the acute phase of arthritis and was higher in collagen-immunized mice that did not develop arthritis. Treatment with 1-MT resulted in an enhanced cellular and humoral immune response and a more dominant polarization to Th1 in mice with arthritis compared with vehicle-treated arthritic mice. The results demonstrated that development of CIA was associated with increased IDO activity and enhanced tryptophan catabolism in mice. Blocking IDO with 1-MT aggravated the severity of arthritis and enhanced the immune responses. These findings suggest that IDO may play an important and novel role in the negative feedback of CIA and possibly in the pathogenesis of rheumatoid arthritis.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Animals Arthritis, Experimental Chromatography, High Pressure Liquid Feedback, Biochemical Humans Indoleamine-Pyrrole 2,3,-Dioxygenase Interleukin-2 Kynuramine/blood Mice Mice, Inbred DBA T-Lymphocytes Tryptophan/analogs and derivatives
Megjelenés:	Arthritis Research and Therapy. - 9 : 3 (2007), p. R50. -
További szerzők:	Koreny Tamás Mikecz Katalin Glant Tibor T. Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Varga John
Internet cím:	elektronikus változat DOI elektronikus változat
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