From gut–brain signalling to AI: Emerging directions in inflammatory bowel disease

Disruption of the gut microbiome may influence central nervous system function and contribute to brain–gut dysfunction in IBD, particularly in patients with overlapping irritable bowel syndrome (IBD–IBS). In IBD, psychological or physical stress can activate gut–brain pathways through the hypothalamic–pituitary–adrenal (HPA) axis, the autonomic nervous system and immune signalling pathways.

Psychological comorbidities may also influence disease outcomes. Anxiety and depression have been associated with increased abdominal pain in patients with IBD and may increase the risk of adverse clinical events, including hospitalisation. Heightened visceral hypersensitivity may also contribute to abdominal pain in patients with IBD–IBS.

Looking ahead, several therapeutic strategies targeting the gut–brain axis are being explored. These include restoring intestinal barrier function through diet and microbiome-directed therapies such as non-absorbable antibiotics, pre-, pro- and post-biotics, and faecal microbiota transplantation. Immune-targeted therapies and neuromodulation approaches, including vagal nerve stimulation, may also help reduce inflammation in IBD.

Serious infection risk across therapies

As treatment options for IBD expand, understanding the safety profile of different therapies remains essential. One nationwide cohort study compared serious infection risk over 1 year in patients treated with aminosalicylates, ustekinumab, tumour necrosis factor (TNF) inhibitors, vedolizumab or Janus kinase (JAK) inhibitors.²

The lowest incidence rate of serious infections was seen with aminosalicylates, followed by ustekinumab, TNF inhibitors, vedolizumab and JAK inhibitors. Compared with aminosalicylates, adjusted hazard ratios for serious infection were lowest with ustekinumab, followed by TNF inhibitors, vedolizumab and JAK inhibitors.

The analysis also identified differences in infection type by treatment class. TNF inhibitors and vedolizumab were associated with skin, upper respiratory and neurologic infections, JAK inhibitors were associated with herpesvirus infections and TNF inhibitors were associated with mycobacterial infections. Concomitant corticosteroids and thiopurine or methotrexate use further increased infection risk.

These findings add useful real-world context to treatment selection in IBD, particularly in patients with additional risk factors for infection.

Artificial intelligence to support clinical decision making

Digital innovation is beginning to influence many areas of gastroenterology. In complex diseases, such as IBD, where treatment strategies are evolving rapidly, AI could help clinicians navigate increasing volumes of information. At ECCO 2026, investigators presented ChatIBD, an AI-based clinical companion designed to support clinicians managing patients with IBD.³

ChatIBD was developed to provide evidence-based responses to questions related to IBD management by retrieving information from more than 30 clinical guidelines from organisations, including ECCO, BSG, AGA, ACG and ESPGHAN. Potential applications include supporting treatment selection, clarifying monitoring strategies and assisting with interpretation of clinical guidelines.

Since its launch in October 2025, ChatIBD has processed 2,642 clinical queries from 578 users across 54 countries in 19 different languages. During its beta phase, the system achieved >95% accuracy across 400 reviewed responses.

Although AI applications in healthcare remain at an early stage, interest in their potential is growing. In gastroenterology, AI is already being explored for tasks such as endoscopic image analysis, disease monitoring and clinical decision support.⁴

Careful validation and oversight will be essential to ensure these systems provide reliable and clinically appropriate information.

Increased risk of metabolic dysfunction–associated steatotic liver disease

Extraintestinal manifestations and comorbidities are an important component of long-term IBD care. Metabolic dysfunction–associated steatotic liver disease (MASLD) is typically linked to metabolic risk factors, including insulin resistance, obesity and dyslipidemia. However, a study presented at ECCO reported that MASLD was more common in patients with IBD, and that it presents with a distinct profile.⁵

In a large population-based cohort of 37,672 patients with IBD, MASLD prevalence was significantly higher than in matched controls (8.0% versus 6.0%; p<0.001), which was also observed in both Crohn’s disease (8.3% versus 5.5%; p<0.001) and ulcerative colitis (7.7% versus 6.6%; p<0.001). Patients with IBD-associated MASLD also presented with lower BMI, liver biomarkers and rates of hypertension, and milder disease activity compared with controls with MASLD, suggesting a distinct disease phenotype.

For clinicians, these findings highlight the importance of considering liver health as part of comprehensive IBD management. Further research is needed to clarify the mechanisms linking IBD with metabolic liver disease and to determine whether targeted screening strategies may benefit patients.

Towards molecular definitions of remission

Treatment targets in ulcerative colitis continue to evolve as clinicians seek more comprehensive measures of disease control. A recent Delphi consensus has proposed comprehensive disease control (CDC) as a composite endpoint to define disease inactivity, integrating multiple clinical, endoscopic and patient-centred endpoints.

At ECCO 2026, investigators explored whether comprehensive disease control corresponded to a molecular signature of minimal residual inflammation.⁶ The study analysed mRNA and mucosa-associated microbiota signatures in patients with ulcerative colitis. The findings suggested that patients achieving CDC showed transcriptomic and microbial patterns consistent with a deeply inactive disease state, with molecular signatures indicating a continuum of mucosal healing.

These results support the development of biomarkers that can objectively detect minimal residual inflammatory activity, although further validation is needed to determine prognostic relevance for long-term outcomes.