1096Enzymatic Modification of Cereal Arabinoxylans: A Structure-Directed Strategy for Precision Prebiotic Design and Intestinal Inflammation Modulation

Xin Jia1,2*, Zhijie Huang1,2, Mingxi Liu1,2 , Xudong Yang1.2, Lijun Yin1,2**

1Beijing Key Laboratory of Functional Food from Plant Resources, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China
2Center of Food Colloids and Delivery for Functionality, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China

Cereal arabinoxylans (AX) are complex non-digestible polysaccharides whose highly polymeric structure and extensive branching patterns significantly limit their fermentation efficiency and immunomodulatory potential. Native AX's structural complexity—characterized by high molecular weight (>300 kDa) and dense arabinose substitution—restricts microbial accessibility in the colon, thereby limiting prebiotic efficacy. This study employed a rational enzymatic engineering approach utilizing glycoside hydrolases (endo-xylanase, α-L-arabinofuranosidase, and feruloyl esterase) to precisely control the degree of polymerization and side-chain substitution patterns, generating arabinoxylan oligosaccharides (AXOS) with defined structural parameters optimized for selective microbial utilization.

In DSS-induced colitis mouse models, enzymatically tailored AXOS demonstrated markedly superior anti-inflammatory efficacy compared to native AX. Integrated multi-omics analyses combining 16S rRNA sequencing, untargeted metabolomics, and targeted SCFA quantification revealed that structure-specific substrate recognition enabled preferential fermentation by beneficial bacteria including Akkermansia, Faecalibaculum , and Dubosiella, while simultaneously suppressing inflammation-associated pathogenic taxa such as Bacteroides and Helicobacter. This selective microbiota modulation occurred through dual mechanisms: ecological competition for nutritional niches and metabolite-mediated inhibition via enhanced production of short-chain fatty acids (acetate, propionate, butyrate) and secondary bile acids. The resulting metabolic reprogramming activated anti-inflammatory signaling pathways (FXR/TGR5, GPR41/43), restored intestinal barrier integrity through upregulation of tight junction proteins (ZO-1, occludin), and significantly reduced hepatic oxidative stress. Our findings establish that enzymatic structural optimization transforms complex polysaccharides into precision prebiotics with targeted immunomodulatory functions. This structure-directed approach offers a systematic framework for developing next-generation dietary interventions that strategically leverage the gut microbiota-metabolite-host axis for managing inflammatory bowel diseases, demonstrating clear translational potential from enzymatic modification through selective microbial enrichment to downstream therapeutic outcomes.