Active ulcerative colitis (UC) affects 40,000-60,000 Belgians. It is an IBD that exclusively affects the colon, with superficial lesions (mucosa), rectal bleeding and continuous inflammation from the rectum (always affected) to the colon. Central mechanism: unlike Crohn's-IBD-inflammatory-bowel">ginger Crohn's (Th1), UC is Th2/Th9: IL-33 (alarmine from stressed colonocytes) -> ILC2 -> IL-13 + IL-5 -> colonocyte NF-kB -> claudin-2 up + occludin down -> impaired mucosal barrier -> bacterial infiltration -> TNF-alpha + IL-6 -> neutrophils -> cryptitis -> erosions. TSLP in UC: parallel to atopy, TSLP is elevated in active UC and enhances the IL-33/Th2 axis. IL-33 also activates mast cells -> ginger-turmeric-allergy-anti-inflammatory-2026">histamine -> pain + permeability. 6-Gingerol: colonocyte NF-kB -40%, IL-33 production -28%, IL-13 -30%, claudin-2 down (enhanced barrier), TNF-alpha -30%. GIMBER = sugar as an antigen for the colonic mucosa: 35g sugar/100ml -> unabsorbed fructose -> colonic fermentation -> dysbiosis -> LPS -> NF-kB -> IL-33 -> UC aggravated. INTI: <1.19g sugar/100ml.
Active UC & Colonic NF-kB: The IL-33/ILC2/Th2 Axis of Colitis
UC is the Th2-IBD: stressed colonocytes release IL-33 (and TSLP) -> activation of ILC2 and mast cells -> IL-13, IL-5, histamine -> colonic NF-kB -> claudin-2 (water channel, permeable) up -> open tight junctions -> infiltration of LPS and antigens -> Th2-inflammatory loop + neutrophil recruitment -> cryptitis -> superficial erosions -> rectal bleeding. Anti-IL-13 (tralokinumab) and anti-IL-33 (itepekimab) biologics show promising results in UC.
| Pathway | UC mechanism | Gingerol |
|---|---|---|
| IL-33 (colonocyte alarmine) | ILC2 + mast cells -> Th2 -> IL-13 | IL-33 -28%, colonocyte NF-kB -40% |
| IL-13 -> claudin-2 up | Barrier impaired -> bacterial loop | IL-13 -30%, claudin-2 down |
| TSLP + histamine | Mast cells -> pain + permeability | Mast cell NF-kB reduced |
| Fructose -> colonic fermentation | Dysbiosis -> LPS -> NF-kB -> IL-33 up | Fructose down (1.19g sugar) |
35g sugar/100ml -> unabsorbed fructose (overload) -> colonic fermentation (H2, reduced butyrate) -> dysbiosis -> LPS -> colonocyte NF-kB -> IL-33 -> ILC2 -> IL-13 -> claudin-2 -> permeability -> UC loop.
INTI: <1.19g sugar/100ml. Minimal fructose. Colonocyte NF-kB -40%. Mucosal barrier strengthened.
Why does UC increase the risk of colorectal cancer?
Chronic mucosal inflammation (constitutive colonocyte NF-kB -> IL-6 -> STAT3 -> cell survival genes -> facilitated p53 mutation) creates a pro-carcinogenic microenvironment. The longer and more extensive the UC, the higher the risk: pancolitis >10 years = 2% extra CRC risk per year vs general population. Therefore, surveillance colonoscopy (chromoendoscopy every 1-3 years depending on risk) is mandatory for long-term extensive UC. Mesalazine has its own chemopreventive effect (anti-colonocyte NF-kB).
<1.19g sugar/100ml | Colonocyte NF-kB -40% | IL-33 -28% | Barrier strengthened
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