Abstract
Inflammatory bowel disease (IBD) is a chronic inflammatory disease, and the incidence of IBD is increasing every year owing to changes in dietary structure. Although the exact pathogenesis of IBD is still unclear, recent evidence suggests that gut dysbiosis is closely associated with IBD pathogenesis. Cheonggukjang is a traditional Korean fermented soybean paste produced using traditional and industrial methods, and contains probiotics, which affect the gut microbiota composition. However, the protective effect of Cheonggukjang against IBD is unknown. In this study, we investigated the bacterial community structure of traditional and commercial Cheonggukjang samples, as well as the protective effect of Cheonggukjang on a dextran sulfate sodium (DSS)-induced colitis mouse model. Traditional and commercial Cheonggukjang were found to contain various type of useful probiotics in their bacterial community structure. Cheonggukjang reduced the progression of DSS-induced symptoms, such as body weight loss, colonic shortening, disease activity index, and histological changes. Further, Cheonggukjang improved the intestinal epithelial barrier integrity on DSS-induced colitis mice. In addition, Cheonggukjang suppressed the expression of proinflammatory cytokines and inflammatory mediators through the inactivation of NF-κB and MAPK signaling pathways. These results indicate that Cheonggukjang exerts protective effects against DSS-induced colitis, suggesting its possible application as a functional food for improving inflammatory diseases.
Highlights
Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the intestine, and its incidence is increasing every year owing to changes in the structure of diets [1–3]
The gut microbiota plays an essential role in the progression of intestinal inflammation in IBD, and it is known that IBD is associated with an imbalance of intestinal bacteria [24]
Probiotics in cheonggukjang have been reported to relieve gut dysbiosis, which is closely associated with IBD [6]
Summary
Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the intestine, and its incidence is increasing every year owing to changes in the structure of diets [1–3]. Many studies have shown that multiple factors, including genetic, microbial, environmental, and immunemediated factors, are associated with IBD, its exact pathogenesis is complex and still unclear [2,5]. Recent evidence suggests that gut dysbiosis is associated with IBD pathogenesis [6]. The mucosal immune system is precisely regulated; disruption of normal mucosal immunity to commensal microbiota results in chronic intestinal inflammation, and, IBD [7,8]. Proinflammatory cytokines, such as IL-1β, IL-6, and TNF-α, which are activated by the nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways, play a crucial role in the colonic mucosal immune response in intestinal inflammation in patients with IBD [9–11]
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