Hyeon-Jeong Jeon

1 Introduction Although the exact underlying causes of inflammatory bowel diseases (IBD) remain unclear, individuals susceptible to IBD commonly exhibit a disrupted intestinal barrier, a dysbiotic microbiome, and consequent dysregulated mucosal immune responses against the dysbiotic microbiome [1-3]. Given the cyclical interdependence of these factors, beneficial modulation of these factors simultaneously is crucial for effective IBD management.