Vatairea guianensis lectin stimulates changes in gene expression and release of TNF-α from rat peritoneal macrophages via glycoconjugate binding

Using a rat model of peritonitis, we herein report the inflammatory effect induced by the lectin isolated from Vatairea guianensis (VGL) seeds in the context of interactions between VGL and both toll-like receptor 4 (TLR4) and tumor necrosis factor receptor 1 (TNFR1). Peritoneal macrophages were stimulated with VGL for dose-dependent gene expression and release of TNF-alpha. In vivo results showed that VGL (1 mg/kg; intraperitoneal) induced peritonitis in female Wistar rats. Leukocyte migration, macrophage activation, and protein leakage were measured 3 and 6 hours after induction. In vitro, peritoneal macrophages were stimulated with VGL for gene expression and TNF-alpha dosage (mean +/- SEM (n = 6), analysis of variance, and Bonferroni's test (P < .05)). In silico, VGL structure was applied in molecular docking with representative glycans. It was found that (a) VGL increases vascular permeability and stimulates leukocyte migration, both rolling and adhesion; (b) lectin-induced neutrophil migration occurs via macrophage stimulation, both in vitro and in vivo; (c) lectin interacts with TLR4 and TNFR1; and (d) stimulates TNF-alpha gene expression (RT-PCR) and release from peritoneal macrophages. Thus, upon lectin-glycan binding on the cell surface, our results suggest that VGL induces an acute inflammatory response, in turn activating the release of peritoneal macrophages via TNF-alpha and TLR and/or TNFR receptor pathways.

Automated summary

In a rat model of peritonitis, the lectin isolated from Vatairea guianensis seeds induces an inflammatory effect through interactions with toll-like receptor 4 (TLR4) and tumor necrosis factor receptor 1 (TNFR1). VGL stimulates gene expression and release of TNF-alpha in peritoneal macrophages, while also inducing peritonitis in female Wistar rats in vivo. The study suggests that VGL induces an acute inflammatory response by interacting with TLR and TNFR receptor pathways, leading to the activation of peritoneal macrophages and TNF-alpha release.