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001-es BibID:	BIBFORM091958
035-os BibID:	(cikkazonosító)107287
Első szerző:	Lima, Carla
Cím:	Natterin an aerolysin-like fish toxin drives IL-1[beta]-dependent neutrophilic inflammation mediated by caspase-1 and caspase-11 activated by the inflammasome sensor NLRP6 / Lima Carla, Falcao Maria Alice Pimentel, Andrade-Barros Aline Ingrid, Seni-Silva Ana Carolina, Grund Lidiane Zito, Balogh Eniko, Conceicao Katia, Queniaux Valerie F., Ryffel Bernhard, Lopes-Ferreira Monica
Dátum:	2021
ISSN:	1567-5769
Megjegyzések:	Natterin is an aerolysin-like pore-forming toxin responsible for the toxic effects of the venom of the medically significant fish Thalassophryne nattereri. Using a combination of pharmacologic and genetic loss-of-function approaches we conduct a systematic investigation of the regulatory mechanisms that control Natterin-induced neutrophilic inflammation in the peritonitis model. Our data confirmed the capacity of Natterin to induce a strong and sustained neutrophilic inflammation leading to systemic inflammatory lung infiltration and revealed overlapping regulatory paths in its control. We found that Natterin induced the extracellular release of mature IL-1? and the sustained production of IL-33 by bronchial epithelial cells. We confirmed the dependence of both ST2/IL-33 and IL-17A/IL-17RA signaling on the local and systemic neutrophils migration, as well as the crucial role of IL-1?, caspase-1 and caspase-11 for neutrophilic inflammation. The inflammation triggered by Natterin was a gasdermin-D-dependent inflammasome process, despite the cells did not die by pyroptosis. Finally, neutrophilic inflammation was mediated by non-canonical NLRP6 and NLRC4 adaptors through ASC interaction, independent of NLRP3. Our data highlight that the inflammatory process dependent on non-canonical inflammasome activation can be a target for pharmacological intervention in accidents by T. nattereri, which does not have adequate specific therapy.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	International Immunopharmacology. - 91 (2021), p. 1-12. -
További szerzők:	Falcao, Maria Alice Pimentel Andrade-Barros, Aline Ingrid Seni-Silva, Ana Carolina Grund, Lidiane Zito Balogh Enikő (1987-) (molekuláris biológus) Conceiçao, Katia Queniaux, Valerie F. Ryffel, Bernhard Lopes-Ferreira, Monica
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM040546
035-os BibID:	PMID:10822092
Első szerző:	Sipka Sándor (laboratóriumi szakorvos)
Cím:	Inhibition of calcineurin activity and protection against cyclosporine A induced cytotoxicity by prednisolone sodium succinate in human peripheral mononuclear cells / Sándor Sipka, Kornélia Szűcs, Sándor Szántó, Ildikó Kovács, Gabriella Lakos, Péter Antal-Szalmás, Gyula Szegedi, Pál Gergely
Dátum:	2000
ISSN:	0162-3109
Megjegyzések:	Free eicosapentaenoic acid (EPA) was found to inhibit dose dependently the chemiluminescence of human neutrophil granulocytes phagocytosing zymosan and their chemotaxis induced by C5a-containing zymosan-activated serum (ZAS) and platelet-activating factor. Rigidification of plasma membranes in the ZAS-treated cells could be observed by measuring the fluorescence anisotropy. The cells were labeled by 3-[p-(6-phenyl-1,3,5-hexatrienoil) phenyl] propionic acid, reporting plasma membrane for determination of membrane fluidity. In resting, nonstimulated neutrophils, EPA dose dependently increased the fluidity of plasma membrane. In zymosan-activated cells, however, after a short fluidization, the basic effect of EPA was a rigidification compared to very low fluorescence anisotropy values of activated control cells. This diminished fluidity, increased membrane stability of plasma membranes can be one of the reasons for the decreased functions (phagocytosis and chemotaxis) of human EPA-treated neutrophils.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Immunopharmacology. - 48 : 1 (2000), p. 87-92. -
További szerzők:	Szűcs Kornélia (1945-) (biokémikus) Szántó Sándor (1968-) (belgyógyász, reumatológus) Kovács Ildikó Lakos Gabriella (1963-) (laboratóriumi szakorvos, transzfúziológus, immunológus) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Szegedi Gyula (1936-2013) (belgyógyász, immunológus) Gergely Pál (1947-) (biokémikus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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