Značaj ekspresije galektina-3 u patogenezi primarnog bilijarnog holangitisa kod miševa

Abstract

Izvod: Uticaj galektina-3 na patogenezu primarnog bilijarnog holangitisa do sada nije ispitivan, a rezultati ove studije jasno pokazuju da Gal-3 može da ima potpuno suprotne efekte na tok bolesti u dva razlišita modela pa izgleda sasvim dokumentovano da uticaj galektina-3 na razvoj i tok bolesti zavisi od dominantnog mehanizma indukcije bolesti. U modelu primarnog bilijarnog holangitisa indukovanog imunizacijom C57BL/6 miševa ksenobiotikom u adjuvansu Gal-3 ima protektivni efekat, ubalažavajći bolest verovatno tako što štiti holangiocite od apoptoze čime smanjuje dostupnost autoantigena i tako ograničava autoimunski proces. Suprotno, u modelu ove bolesti izazvane bakterijom Novosphingobium aromaticivorans odsustvo galektina-3 gotovo da čini miševe rezistentnim na razvoj RVS najverovatnije zbog neadekvatne aktivacije dendritskih ćelija bakterijom u odsustvu galektina-3, usled čega izostaje i aktivacija svih ostalih ćelija (NKT i NK ćelija, T limfocita) koje učestvuju u razvoju oštećenja bilijarnih kanala.

Abstract: The impact of galectin-3 in the pathogenesis of primary biliary cholangitis has not been studied, and the results of this study clearly show that Gal-3 can have completely opposite effects on the course of the disease in two different induction models looks quite documented that the effect of galectin-3 in the development and course of the disease depends on the prevalent mechanism for the induction of the disease. In the model of primary of biliary cholangitis induced by immunizing C57BL/6 mice with xenobiotics in adjuvant, Gal-3 has a protective effect, mitigating disease probably by protecting from apoptosis holangiocite thus reducing the availability of autoantigens, thus limiting the autoimmune process. Contrary, in the model of this disease caused by bacteria Novosphingobium aromaticivorans absence of galectin-3 almost makes the mice resistant to the development of PBC most likely due to inadequate activation of dendritic cells by the bacteria in the absence of galectin-3, and subsequent reduced activation of other cells (NKT and NK cells, T lymphocytes) that participate in the development of biliary duct damage.