Active Ulcerative Colitis Belgium 2025: NF-kB Colonocytes, IL-33 & Ginger

SCIENTIFIC SUMMARY

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)
GIMBER = fructose as UC enhancer.
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.
Medical note: Active UC requires specialized treatment: 5-ASA (mesalazine) for mild-moderate forms, corticosteroids (flares), immunosuppressants (azathioprine), biologics (anti-TNF, vedolizumab, ustekinumab, ozanimod, etrasimod). Colectomy is curative for UC (unlike Crohn's). INTI does not replace this treatment but can provide complementary support.
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).

INTI: Anti-IL-33/Colonocyte NF-kB for UC

<1.19g sugar/100ml | Colonocyte NF-kB -40% | IL-33 -28% | Barrier strengthened

Discover INTI

Related articles

Read more about related topics :

Recommended pages

Explore more about INTI :

Back to blog