Alginate oligosaccharides enhance gut microbiota and intestinal barrier function, alleviating host damage induced by deoxynivalenol in mice.

Abstract

Background: Alginate oligosaccharides (AOS) exhibits notable effects in terms of anti-inflammatory, antibacterial, and antioxidant properties. Deoxynivalenol (DON) has the potential to trigger intestinal inflammation by upregulating proinflammatory cytokines and apoptosis, thereby compromising the integrity of the intestinal barrier function and perturbing the balance of the gut microbiota.

Objectives: We assessed the impact of AOS on mitigating DON-induced intestinal damage and systemic inflammation in mice.

Methods: After a one-week acclimatization period, the mice were divided into four groups. For three weeks, the AOS and AOS + DON groups were gavaged daily with 200 μl of AOS (200 mg/kg body weight (BW)), while the CON and DON groups received an equivalent volume of sterile Phosphate Buffered Saline (PBS). Subsequently, for one week, the DON and AOS + DON groups received 100 μl of DON (4.8 mg/kg BW) daily, whereas the CON and AOS groups continued receiving PBS.

Results: After administering DON via gavage to mice, there was a significant decrease (P < 0.05) in body weights compared to the control (CON) group. Interestingly, AOS exhibited a tendency to mitigate this weight loss in the AOS + DON group. In the feces of mice treated with both AOS and DON, the concentration of DON significantly increased (P < 0.05) compared to the DON group alone. Histological analysis revealed that DON exposure caused increased intestinal damage, including shortened villi and eroded epithelial cells, which was ameliorated by pre-supplementation with AOS, alleviating harm to the intestinal barrier function. In both jejunum and colon tissues, DON exposure significantly reduced (P < 0.05) the expression of tight junction proteins (Claudin and Occludin in the colon) and the mucin protein Mucin 2 (MUC2), compared to the CON group. Prophylactic administration of AOS alleviated these reductions, thereby improving the expression levels of these key proteins. Additionally, AOS supplementation protected DON-exposed mice by increasing the abundance of probiotics such as Bifidobacterium, Faecalibaculum, and Romboutsia. These gut microbes are known to enhance (P < 0.05) anti-inflammatory responses and the production of short-chain fatty acids (SCFAs), including total SCFAs, acetate, and valerate, compared to the DON group.

Conclusions: This study unveils AOS not only enhance gut microbiota and intestinal barrier function but also significantly mitigate DON-induced intestinal damage.