Dairy propionibacteria prevent the proliferative effect of plant lectins on SW480 cells and protect the metabolic activity of the intestinal microbiota in vitro

- Food may possess antinutritional factors such as plant lectins that cause deleterious effects on gut physiology.
- Concanavalin A and jacalin stimulate proliferation of SW480 colorectal cancer cell line and decrease colonic fermentation.
- Propionibacteria bound to these lectins and decreased the incidence of lectin-induced alterations in vitro.

Plant lectins are specific carbohydrate-binding proteins that are widespread in legumes such as beans and pulses, seeds, cereals, and many plants used as farm feeds. They are highly resistant to cooking and digestion, reaching the intestinal lumen and/or blood circulation with biological activity. Since many legume lectins trigger harmful local and systemic reactions after their binding to the mucosal surface, these molecules are generally considered anti-nutritive and/or toxic substances. In the gut, specific cell receptors and bacteria may interact with these dietary components, leading to changes in intestinal physiology. It has been proposed that probiotic microorganisms with suitable surface glycosidic moieties could bind to dietary lectins, favoring their elimination from the intestinal lumen or inhibiting their interaction with epithelial cells. In this work, we assessed in vitro the effects of two representative plant lectins, concanavalin A (Con A) and jacalin (AIL) on the proliferation of SW480 colonic adenocarcinoma cells and metabolic activity of colonic microbiota in the absence or presence of Propionibacterium acidipropionici CRL 1198. Both lectins induced proliferation of colonic cells in a dose-dependent manner, whereas ConA inhibited fermentative activities of colonic microbiota. Pre-incubation of propionibacteria with lectins prevented these effects, which could be ascribed to the binding of lectins by bacterial cells since P. acidipropionici CRL 1198 was unable to metabolize these proteins, and its adhesion to colonic cells was reduced after reaction with Con A or AIL. The results suggest that consumption of propionibacteria at the same time as lectins could reduce the incidence of lectin-induced alterations in the gut and may be a tool to protect intestinal physiology.