o:1941 Uloga osovine IL-33/ST2 u imunopatogenezi eksperimentalnog akutnog oštećenja želuca Тhe role of the IL-33/ST2 axis in the immunopathogenesis of experimental acute gastric injury : doctoral dissertation sr Peptička ulkusna bolest predstavlja značajan globalni zdravstveni problemzbog visoke učestalosti i ozbiljnih kliničkih komplikacija. Bolje razumevanjeinflamacijskih puteva koji učestvuju u oštećenju sluznice želuca može otvoriti novemogućnosti za ciljane terapijske intervencije. Eksperimentalna manipulacija IL-33/ST2 osovine pokazala je da može uticati na tok inflamacije i oštećenja epitela ugastrointestinalnom traktu.Cilj studije je da se ispita efekat delecije ST2 na različite tokoveinflamacije i mehanizme ćelijske smrti u eksperimentalnom modelu akutnog oštećenjaželuca.Akutno oštećenje želuca izazvano je jednokratnom primenom 80% etanolaoralnom gavažom kod miševa sa nedostatkom gena za ST2 i miševa čistog soja BALB/c.Nakon indukcije oštećenja sprovedena je makroskopska i p atohistološka procenaintenziteta tkivnog oštećenja. Analiziran je uticaj delecije ST2 na modulacijuimunskog odgovora i puteva ćelijske smrti u oštećenom tkivu želuca, dok jerekombinantni mišji IL-33 aplikovan u ciljnim grupama radi funkcionalne potvrde.Delecija ST2 ublažava akutno oštećenje želuca kod miševa inhibicijom NF-κB i NLRP3 signalnih puteva u tkivu želuca, što je praćeno smanjenom infiltracijomćelija urođene i stečene imunosti, kao i sniženom produkcijom proinflamacijskihcitokina. Takođe, delecija ST2 ograničava apoptozu epitelnih ćelija, dok primenarekombinantnog IL-33 pogoršava oštećenje sluznice želuca, potvrđujući patogenuulogu IL-33/ST2 osovine.Dobijeni rezultati ukazuju da nedostatak ST2 gena ublažava akutno oštećenježeluca i ciljanje IL-33/ST2 osovine predstavlja potencijalno obećavajuću strategiju zalečenje peptične ulkusne bolesti želuca. Peptic ulcer disease represents a significant global health problem due to its highprevalence and serious clinical complications. A better understanding of the inflammatorypathways involved in gastric mucosal injury may open new opportunities for targetedtherapeutic interventions. Experimental manipulation of the IL-33/ST2 axis has been shown toinfluence the course of inflammation and epithelial damage in the gastrointestinal tract.The aim of this study was to investigate the effect of ST2 deletion on differentinflammatory pathways and mechanisms of cell death in an experimental model of acute gastricinjury.Acute gastric injury was induced by a single oral gavage of 80% ethanol in wild-typeand ST2-deficient BALB/c mice. Following injury induction, macroscopic andhistopathological assessments of tissue damage severity were performed. The impact of ST2deletion on immune response modulation and cell death pathways in damaged gastric tissuewas analyzed, while recombinant murine IL-33 was administered to selected groups forfunctional validation.ST2 deletion attenuated acute gastric injury in mice by inhibiting NF-κB and NLRP3signaling in gastric tissue, which was accompanied by reduced infiltration of innate andadaptive immune cells and decreased production of pro-inflammatory cytokines. In addition,ST2 deletion limited epithelial cell apoptosis, whereas administration of recombinant IL-33exacerbated gastric mucosal damage, confirming the pathogenic role of the IL-33/ST2 axis.These findings indicate that ST2 deficiency alleviates acute gastric injury and thattargeting the IL-33/ST2 axis represents a promising strategy for the treatment of peptic ulcerdisease. - 91552100 199552777 91552101 8960 2026-09-16T10:43:59.053Z 45 no 46 Irfan, 1993- Ćorović 125160969 2026 63 mentor Bojana, 1984- Simović Marković 27316327 2026 63 član komisije Gordana, 1976- Radosavljević 13591143 2026 63 član komisije Jelena, 1977- Pantić 25899623 2026 63 član komisije Dušan, 1980- Popović 34769767 2026 94 lista 2397994 http://phaidrakg.kg.ac.rs/o:1941 no yes 12 2026-09-16T10:43:59.320Z 70 IL-33/ST2 osovina, akutno oštećenje želuca, NF-κB, NLRP3inflamazom, ćelijska smrt. IL-33/ST2 axis, аcute gastric injury, NF-κB, NLRP3 inflammasome, celldeath. 616.33-002.1-092-097(043.3) 1738 34A05 2026