A multicomponent mycotoxin deactivator modifies the response of the jejunal mucosal and cecal bacterial community to deoxynivalenol contaminated feed and oral lipopolysaccharide challenge in chickens1.
Mycotoxin deactivators are a widely used strategy to abrogate negative effects of mycotoxin-contaminated feed. It has not been adequately evaluated whether these deactivators may detoxify bacterial toxins in the intestinal lumen and subsequently lower the inflammatory response in chickens. The present objective was to study the effect of a multicomponent mycotoxin deactivator (B), containing a bentonite and a bacterial strain capable to enzymatically biotransform trichothecenes especially deoxynivalenol (DON), when supplemented to a DON-contaminated feed in combination with an oral lipopolysaccharide challenge on visceral organ size, expression of innate immune genes and mucosal permeability in the small intestine as well as on the cecal bacterial composition and metabolites in broiler chickens. Eighty 1-d-old male chickens were randomly allotted to four treatment groups in two replicate batches (n = 10/treatment/replicate): 1) basal diet without DON (CON), 2) CON diet supplemented with B (2.5 mg B/kg feed) (CON-B), 3) CON diet contaminated with 10 mg DON/kg feed (DON), and 4) DON diet supplemented with 2.5 mg B/kg feed (DON-B). In half of the chickens per treatment, effects were assessed under nonchallenge conditions, whereas in the other half of birds, to increase their intestinal bacterial toxin load, effects were tested after an oral challenge with 1 mg LPS/kg BW from Escherichia coli O55:B5 on the day before sampling. DON reduced (P < 0.05) the weight of bursa fabricii and thymus. DON increased the expression level of intestinal alkaline phosphatase at the duodenal mucosa (P = 0.027) but did not modify jejunal gene expression and mucosal permeability. The LPS challenge decreased the jejunal MUC2 expression but increased ZO1 and IL6 expression compared to the unchallenged animals (P < 0.05). DON × B interactions indicated lower expression of IL10 in duodenum and NFKB in jejunum with the B diet but higher expression with the DON-B diet (P = 0.050). Furthermore, the B lowered jejunal expression of NFKB and IL6 but only in LPS-challenged chickens (P < 0.05). Alterations in the cecal microbiota composition and VFA profile were likely associated with alterations in host physiology in the small intestine caused by DON, B, and LPS. According to the present data, B appeared to have potential to detoxify antigens other than DON in the intestinal lumen of chickens, whereby the toxin load may limit the efficacy of B to modify the intestinal and systemic response as indicated by interactions of DON, B, and LPS.