Abstract
The low viability during gastrointestinal transit and poor mucoadhesion considerably limits the effectiveness of Ligilactobacillus salivarius Li01 (Li01) in regulating gut microbiota and alleviating inflammatory bowel disease (IBD). In this study, a delivery system was designed through layer-by-layer (LbL) encapsulating a single Li01cell with chitosan and alginate. The layers were strengthened by cross-linking to form a firm and mucoadhesive shell (~10 nm thickness) covering the bacterial cell. The LbL Li01 displayed improved viability under simulated gastrointestinal conditions and mucoadhesive function. Almost no cells could be detected among the free Li01 after 2 h incubation in digestive fluids, while for LbL Li01, the total reduction was around 3 log CFU/mL and the viable number of cells remained above 6 log CFU/mL. Besides, a 5-fold increase in the value of rupture length and a two-fold increase in the number of peaks were found in the (bacteria-mucin) adhesion curves of LbL Li01, compared to those of free Li01. Oral administration with LbL Li01 on colitis mice facilitated intestinal barrier recovery and restoration of the gut microbiota. The improved functionality of Li01 by LbL encapsulation could increase the potential for the probiotic to be used in clinical applications to treat IBD; this should be explored in future studies.
Highlights
Inflammatory bowel disease (IBD) constitutes an emerging set of diseases, with increasing incidence and prevalence worldwide[1]
Li01 was decorated with different numbers of layers, with the Chitosan has been shown to be highly adhesive to mucin, maximum of three chitosan-alginate (CA) bilayers
The process of LbL encapsulation entails the formation of nanolaminated biopolymer coatings enveloping the probiotic bacteria
Summary
Inflammatory bowel disease (IBD) constitutes an emerging set of diseases, with increasing incidence and prevalence worldwide[1]. IBD includes ulcerative colitis and Crohn’s disease, which are chronic, life-long, and relapsing diseases of the gastrointestinal (GI) tract caused by a range of genetic and environmental factors[2]. IBD still remains incurable despite many clinically available therapeutic interventions, and the exact mechanism of IBD development remains unknown. Recent studies have found dysregulated interactions among the intestinal bacteria, the gut barrier, and the intestinal-associated immune system in patients with IBD. The diversity of the gut microbiota and the relative abundance of Firmicutes, Bacteroidetes and Actinobacteria has been found to be decreased in patients with IBD2,3. The gut microbiome is considered a potential, novel target for IBD treatment[4,5]
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