<abstract xmlns="http://www.w3.org/1999/xhtml"><p>Toll-like receptor-4 (TLR-4) is a member of evolutionarily conserved type I transmembrane proteins that can initiate sterile inflammatory cascade in the pancreas. Expression of TLR-4 is up-regulated in pancreatic tissue, as well as, on peripheral blood innate immune cells in human and experimental models of acute pancreatitis. TLR-4 plays important pro-inflammatory roles during development of acute pancreatitis: it recognize alarmins released from injured acinar cells and promotes activation and infiltration of innate immune cells after the premature and intraacinar activation of tripsinogen. Galectin-3 is β-galactoside-binding lectin that plays pro-inflammatory roles in a variety autoimmune diseases, acute bacterial infections and during tumorigenesis. It is reported that Galectin-3 is alarmin in experimental models of neuroinflammation and binds to TLR-4 promoting the pro-inflammatory phenotype of microglia. Also, in experimental model of acute pancreatitis Galectin-3 is colocalized with TLR-4 on innate inflammatory cells resulted in enhanced production of inflammatory cytokines, TNF-α and IL-1β, increased infiltration of pro-inflammatory N1 neutrophils, macrophages and dendritic cells and increased damage of pancreatic tissue. This review paper discusses the role of TLR-4/Gal-3 axis in the pathogenesis of acute pancreatitis.</p></abstract>

Toll-like receptor-4 (TLR-4) is a member of evolutionarily conserved type I transmembrane proteins that can initiate sterile inflammatory cascade in the pancreas. Expression of TLR-4 is up-regulated in pancreatic tissue, as well as, on peripheral blood innate immune cells in human and experimental models of acute pancreatitis. TLR-4 plays important pro-inflammatory roles during development of acute pancreatitis: it recognize alarmins released from injured acinar cells and promotes activation and infiltration of innate immune cells after the premature and intraacinar activation of tripsinogen. Galectin-3 is β-galactoside-binding lectin that plays pro-inflammatory roles in a variety autoimmune diseases, acute bacterial infections and during tumorigenesis. It is reported that Galectin-3 is alarmin in experimental models of neuroinflammation and binds to TLR-4 promoting the pro-inflammatory phenotype of microglia. Also, in experimental model of acute pancreatitis Galectin-3 is colocalized with TLR-4 on innate inflammatory cells resulted in enhanced production of inflammatory cytokines, TNF-α and IL-1β, increased infiltration of pro-inflammatory N1 neutrophils, macrophages and dendritic cells and increased damage of pancreatic tissue. This review paper discusses the role of TLR-4/Gal-3 axis in the pathogenesis of acute pancreatitis.

The Role of TLR-4 and Galectin-3 Interaction in Acute Pancreatitis

Faculty of Medical Sciences, Center for Molecular Medicine and Stem Cell Research

Faculty of Medical Sciences, Department of Pathology

Faculty of Medical Sciences, Department of Surgery

Faculty of Medical Sciences, Department of Pathophysiology

Experimental and Applied Biomedical Research (EABR)

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

{"article-title":"The Role of TLR-4 and Galectin-3 Interaction in Acute Pancreatitis"}

Toll-like receptor-4 (TLR-4) is a member of evolutionarily conserved type I transmembrane proteins that can initiate sterile inflammatory cascade in the...

The Role of TLR-4 and Galectin-3 Interaction in Acute Pancreatitis

Online veröffentlicht: 05. Nov. 2020

Seitenbereich: -

Eingereicht: 04. Nov. 2019

Akzeptiert: 20. Nov. 2019

DOI: https://doi.org/10.2478/sjecr-2019-0067

Schlüsselwörter
TLR-4, Galectin-3, acute pancreatiti

© 2019 Milica Dimitrijevic Stojanovic et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

The Role of TLR-4 and Galectin-3 Interaction in Acute Pancreatitis

Online veröffentlicht: 05. Nov. 2020

Seitenbereich: -

Eingereicht: 04. Nov. 2019

Akzeptiert: 20. Nov. 2019

DOI: https://doi.org/10.2478/sjecr-2019-0067

SchlüsselwörterTLR-4, Galectin-3, acute pancreatiti

© 2019 Milica Dimitrijevic Stojanovic et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Schlüsselwörter
TLR-4, Galectin-3, acute pancreatiti