2'-Fucosyllactose and 3-Fucosyllactose Alleviates Interleukin-6-Induced Barrier Dysfunction and Dextran Sodium Sulfate-Induced Colitis by Improving Intestinal Barrier Function and Modulating the Intestinal Microbiome.
Yeon-Ji KimHan-Hae KimChul-Soo ShinJong-Won YoonSeon-Min JeonYoung-Ha SongKwang-Youn KimKyungho KimPublished in: Nutrients (2023)
Ulcerative colitis is an inflammatory bowel disease (IBD) with relapsing and remitting patterns, and it is caused by varied factors, such as the intestinal inflammation extent and duration. We examined the preventative effects of human milk oligosaccharides (HMOs) on epithelial barrier integrity and intestinal inflammation in an interleukin (IL)-6-induced cell model and dextran sodium sulfate (DSS)-induced acute mouse colitis model. HMOs including 2'-fucosyllactose (FL) and 3-FL and positive controls including fructooligosaccharide (FOS) and 5-acetylsalicylic acid (5-ASA) were orally administrated once per day to C57BL/6J mice with colitis induced by 5% DSS in the administered drinking water. 2'-FL and 3-FL did not affect the cell viability in Caco-2 cells. Meanwhile, these agents reversed IL-6-reduced intestinal barrier function in Caco-2 cells. Furthermore, 2'-FL and 3-FL reversed the body weight loss and the remarkably short colon lengths in DSS-induced acute colitis mice. Moreover, 2'-FL and 3-FL obviously protected the decreasing expression of zonula occluden-1 and occludin in colon tissue relative to the findings in the DSS-treated control group. 2'-FL and 3-FL significantly reduced IL-6 and tumor necrosis factor-α levels in serum relative to the control findings. The summary of these results shows that HMOs prevent colitis mainly by enhancing intestinal barrier function and advancing anti-inflammatory responses. Therefore, HMOs might suppress inflammatory responses and represent candidate treatments for IBD that protect intestinal integrity.
Keyphrases
- human milk
- ulcerative colitis
- drinking water
- induced apoptosis
- oxidative stress
- weight loss
- low birth weight
- stem cells
- signaling pathway
- type diabetes
- rheumatoid arthritis
- poor prognosis
- cell cycle arrest
- risk assessment
- systemic lupus erythematosus
- mouse model
- metabolic syndrome
- long non coding rna
- disease activity
- mesenchymal stem cells
- preterm birth
- insulin resistance
- health risk assessment
- glycemic control
- cell death
- obese patients
- roux en y gastric bypass
- bone marrow
- cell proliferation