Several abstracts provided important insights into the biological mechanisms underlying IBD heterogeneity. A study investigating host–microbe interactions demonstrated how Escherichia coli can shape mucosal B-cell responses, potentially influencing susceptibility to IBD (DOP144 Escherichia coli shapes intestinal B-cell responses and influences susceptibility to Inflammatory Bowel Disease). Complementing this, advanced transcriptomic analyses identified distinct molecular pathways associated with disease activity and long-term prognosis in Ulcerative Colitis, supporting the concept of biologically defined disease subtypes (DOP049 Transcriptomic profiling reveals divergent molecular pathways underlying Ulcerative Colitis disease activity and prognostic severity).

Genetic determinants of disease phenotype were further explored in a large genome-wide association study identifying HLA-DRB1*01:03 as a key variant associated with perianal Crohn’s Disease severity (DOP026 HLA-DRB1*01:03 is associated with perianal Crohn’s disease phenotype and severity). Expanding on molecular risk stratification, integrated immune and molecular profiling approaches identified IBD lesions at increased risk of advanced neoplasia, highlighting the potential of combining multi-layered data for early cancer risk prediction (DOP111 Integrated Immune and Molecular Profiling Identifies Inflammatory Bowel Disease Lesions at Risk for Advanced Neoplasia).

Together, these findings reinforce the transition from a phenotype-based to a molecularly stratified approach in IBD.

The integration of multi-omic and computational approaches was a prominent theme. A machine learning-based study identified blood gene signatures capable of predicting endoscopic disease severity in Ulcerative Colitis, offering a promising non-invasive alternative to endoscopy (DOP097 Discovery and external validation of machine learning-derived blood gene signatures for predicting endoscopic disease severity in Ulcerative Colitis).

Similarly, histological signatures integrated with imaging and molecular markers were shown to predict intestinal barrier dysfunction and adverse outcomes, highlighting the value of multi-level biomarker integration (DOP018 Histologic Signatures as Predictors of Intestinal Barrier Dysfunction in IBD: Integration with Endoscopic and Molecular Markers).

Pharmacokinetic and transcriptomic profiling in Acute Severe Ulcerative Colitis revealed that higher infliximab exposure is associated with mucosal healing and distinct molecular signatures, providing a mechanistic basis for therapeutic optimisation (DOP066 Pharmacokinetics and transcriptomic analysis reveal the molecular signature of mucosal healing in patients with Acute Severe Ulcerative Colitis treated with infliximab (PROTOS)).

Several studies addressed emerging therapies and optimisation strategies. A phase 2 trial evaluating the IL-23 inhibitor picankibart demonstrated promising efficacy and safety in moderate-to-severe Ulcerative Colitis (DOP058 Efficacy and safety of picankibart in patients with moderately to severely active ulcerative colitis: a randomised, double-blind, placebo-controlled phase 2 trial).

In Crohn’s Disease, combination therapy with adalimumab and partial enteral nutrition improved clinical outcomes compared with biologic monotherapy, suggesting a potential role for nutritional–pharmacological synergy (DOP100 Combination treatment with adalimumab and partial enteral nutrition compared with adalimumab monotherapy in adults with active Crohn’s disease: The BIOPIC study).

Long-term data from the LIR!C trial provided important insights into treatment strategies, showing that ileocaecal resection remains a valid alternative to infliximab, with sustained outcomes over 10 years (DOP006 Ileocaecal resection versus infliximab for ileal Crohn’s disease: 10-year follow-up of the LIR!C trial).

Additional selected abstracts further emphasised the importance of optimising therapeutic strategies and refining treatment positioning in the era of precision medicine (DOP135 Bowel damage and disability in Crohn’s disease in the first year after diagnosis – results from the CROCO study).

Real-world data continue to inform clinical decision-making. A propensity score-matched analysis from the PANIC cohort evaluated ustekinumab and vedolizumab in fistulising Crohn’s Disease, addressing an important gap in evidence beyond anti-TNF therapy (DOP084 Ustekinumab and vedolizumab in the treatment of fistulising Crohn’s disease: a propensity score-matched analysis from the prospective Persistence Australian National Inflammatory Bowel Disease Cohort (PANIC5) study).

The TACTIC-UC study demonstrated that endoscopy-driven treat-to-target optimisation leads to improved endoscopic and histological outcomes, even in patients with minimal symptoms, reinforcing the importance of objective disease assessment (DOP028 Treat-to-target optimization is effective on endoscopic and histologic outcomes in a real-life cohort of ulcerative colitis – the TACTIC-UC Study).

In special populations, updated data from the DUMBO registry confirmed that disease activity during pregnancy remains a relevant clinical issue, emphasising the need for careful monitoring and management (DOP044 Prevalence and factors associated with inflammatory bowel disease (IBD) activity during pregnancy: updated data from the Dumbo registry).

Beyond intestinal inflammation, new data highlighted systemic implications of IBD. A large population-based study demonstrated an increased risk of metabolic dysfunction-associated steatotic liver disease in patients with IBD, independent of traditional metabolic risk factors, expanding our understanding of disease burden (DOP121 Patients with IBD Are at Increased Risk of Metabolic Dysfunction–Associated Steatotic Liver Disease, Independent of Classic Metabolic Risk Factors).

Innovative experimental models are advancing our understanding of disease mechanisms. A bioengineered 3D model of gut barrier function provided new insights into host–fungal interactions and inflammasome activation in Crohn’s Disease, offering a platform for future therapeutic development (DOP078 Development of a bioengineered 3D model of gut barrier defence against Candida albicans invasion and inflammasome activation in Crohn’s Disease).

The selected abstracts from ECCO 2026 reflect a clear shift towards precision medicine in IBD, integrating molecular profiling, advanced biomarkers and real-world evidence to guide individualised care. From mechanistic discoveries to clinical application, these studies highlight the ongoing transformation of IBD management, with a growing emphasis on early prediction, targeted intervention and long-term disease modification.