Source: IBS Days 2026.

 

From 15 to 17 June 2026, Gut Microbiota for Health attended IBS Days in Bologna, Italy, which celebrated its 10th anniversary. Sessions at the conference cross-cut basic, translational, and clinical science in IBS, including epidemiology, genetic influences, gut microbiota, immune pathways, dietary and infectious triggers, biomarker advances, and non-pharmacological interventions.

 

Is it IBS or a different diagnosis?

It is common for IBS to co-occur with other conditions in which the gut microbiome is directly or indirectly involved. IBS-like symptoms are reported in 30% of IBD patients, particularly those with Crohn’s disease, despite endoscopic remission. An additional risk factor is that approximately 10% of individuals develop IBS following gastrointestinal infection. Increased intestinal permeability is another feature shared by IBS and IBD and may also be triggered by enteric infections. Finally, the immune alterations underlying Crohn’s disease, as well as those induced by acute gastroenteritis, may persist over time as low-grade inflammation, which is considered one of the key mechanisms involved in IBS1.

Proposed pathways underlying symptom development in patients with IBD with IBS-like symptoms. Source: Lin Chang’s talk at IBS Days 2026.

 

A global study of 54,127 adults (49.1% women) across 26 countries revealed that greater overlap of disorders of gut-brain interaction (DGBI) across one or more GI regions (esophageal, gastroduodenal, bowel, and anorectal) may lead to increased disease severity and poorer quality of life2. In addition, female sex and gender-related factors influence DGBI prevalence, symptom patterns, and comorbidities. IBS also overlaps with endometriosis, with a pooled prevalence of IBS in women with endometriosis of 23.4%3. Endometriosis may share mechanisms with IBS involving sensitization, inflammation, mast cell activation, and an altered gut microbiome. Importantly, IBS may be misdiagnosed in women with ovarian cancer before the age of 50 (hazard ratio = 1.07, 95% CI: 1.04-1.10, p<0.01)4. In that regard, National Institute for Health and Care Excellence’s guidelines recommend carrying out appropriate tests for ovarian cancer in any woman of 50 or over who has experienced symptoms that suggest IBS within the last 12 months5.

Last, bile acid diarrhea (BAD) should be considered in any child or adult presenting with chronic diarrhea/IBS with diarrhea-particularly postprandial diarrhea, with defecatory urgency and episodes of fecal incontinence-once infectious and inflammatory causes are ruled out. Recent findings suggest that BAD is associated with a gut microbiome with decreased expression of bile acid thiol ligase (involved in the transformation of primary to secondary bile acids) and decreased sulfatases, highlighting the potential of targeting microbial taxa for future treatments6,7. The role of small intestinal bacterial overgrowth, pancreatic exocrine insufficiency, and symptomatic uncomplicated diverticular disease and their link to IBS remain uncertain.

 

The epithelial and vascular gut barriers are compromised in IBS

The gut barrier is a “four-in-one” system composed progressively of the gut microbiota, mucus, epithelial and vascular barriers. Elevated intestinal permeability is common in children and adults with IBS, especially in the diarrhea and post-infectious subtypes8. It may arise from increased epithelial and vascular permeability and contribute to clinical manifestations in patients with IBS9.

Experimental findings showed the existence of a new choroid plexus vascular barrier (PVB) whose role becomes evident only during inflammation. When the gut vascular barrier, the body’s primary protective system against the external world, is compromised (e.g., during gastroenteritis), the PVB serves as a secondary protective mechanism for the central nervous system against systemic inflammation10. Unpublished findings in mice showed rifaximin protected the intestinal barrier from chemotherapy-induced mucositis, preventing the depletion of health-associated taxa. Muribaculum intestinale supplementation recapitulated the effects of rifaximin and reduced intestinal damage, despite not changing gut microbiota composition.

The plexus vascular barrier is sort of a secondary protection that intervenes when the gut vascular barrier is no longer functional or altered.
Source: Maria Rescigno’s talk at IBS Days 2026.

Diet may shape the epithelial barrier, which regulates passage from the intestinal lumen into the lamina propria, and the gut vascular barrier, which controls the systemic dissemination of bacteria. A diet low in dietary fibers and rich in emulsifiers (particularly carboxymethylcellulose and polysorbate 80), saturated fats, and salt has been repeatedly associated with impaired intestinal permeability, increased pathogenic bacterial taxa, and increased inflammatory response11. In contrast, increasing complex soluble fibers (i.e., pectin and b-glucan) supports mucus production and gut barrier homeostasis. When appropriate, reducing dietary FODMAPs may improve colonic barrier dysfunction and mast cell recruitment and activation in patients with IBD-D12. Nutraceuticals such as sodium butyrate13, glutamine14, a blend of prebiotics with pea protein and grape seed extract15, and selected probiotics16,17,18 show promise in restoring intestinal epithelial and vascular barriers in patients with IBS.

Therapeutic interventions for disorders of gut-brain interaction that impact intestinal permeability.
Source: Giovanni Barbara’s talk at IBS Days 2026.

 

Advances in understanding how the gut microbiome influences the brain and auto-brewery syndrome

The roots of high psychiatric comorbidity in IBS are poorly understood but likely involve multiple pathways. Recent insights point to the role of outer membrane vesicles (OMVs) produced by Gram-negative gut bacteria in brain and behavior. These vesicles are critical for the survival of commensal bacteria, but they can also signal to the host in two ways. Preclinical studies have revealed that oral administration of OMVs increases blood-brain barrier permeability, allowing the release of the vesicle interior, consisting of a variety of cytoplasmic molecules and DNA fragments, into the brain. This results in alterations in brain chemistry and function19. The second mechanism involves activation of the vagus nerve via toll-like receptors20. Limitations of current knowledge include the cytokine storm induced by lipopolysaccharide from Gram-negative bacteria, contamination, dose-relevance, and the translational gap between rodent studies and human disease.

Gram-negative outer membrane vesicles are an important component of the microbiome-gut-brain axis and offer novel therapeutic approaches for managing altered brain function in IBS and behavioral disorders.
Source: Stephen Collins’ talk at IBS Days 2026.

Increasing awareness of auto-brewery syndrome (ABS), or gut fermentation syndrome, and improved diagnostic approaches have led to a growing number of reported cases worldwide. The pathogenesis of ABS is multifactorial and involves an altered gut microbiome with overgrowth of fermenting yeasts and certain bacterial taxa capable of producing ethanol. The typical patient profile of a patient with ABS ranges from episodic neurocognitive and behavioral symptoms resembling alcohol intoxication to chronic fatigue, cognitive impairment, and reduced quality of life. Diagnosis is challenging and requires careful exclusion of exogenous alcohol consumption. Management includes dietary sugar restriction, targeted antimicrobial or antifungal therapy, correction of underlying predisposing factors, and microbiota-directed interventions21. Emerging evidence suggests a potential role of probiotics and fecal microbiota transplantation in selected refractory cases22.

Potential therapeutic approaches for auto-brewery syndrome.
Source: William Fusco’s talk at IBS Days 2026.

 

Non-pharmacological interventions targeting the microbiome for IBS

Diet and nutrition are no longer considered footnotes in the management of IBS. The end goal of dietary management of IBS is to avoid over-restriction and achieve maximum diet variety while maintaining symptom control. Dietary modification is the preferred first-line management approach for most patients, with over 80% reporting that food triggers or worsens their symptoms. Clinical guidelines recommend traditional dietary advice as the initial intervention, yet only approximately 40% of patients respond. Nonresponders are typically escalated to the low-FODMAP diet, which achieves a clinical response in 50–70% of cases. Recent randomized trial data23,24,25 support the Mediterranean diet as another first-line dietary option for managing IBS before escalating to complex second-line treatments (e.g., the low-FODMAP diet).

The low-FODMAP diet is effective for IBS but removes some foods high in fiber and limits dietary variety, with potentially detrimental effects on the gut microbiome. The evolution of the low FODMAP diet is to minimize restriction, simplify the treatment plan, and improve food-related quality of life. However, the low-FODMAP gentle approach is based mainly on clinical observation. It has only been formally studied in a small pilot randomized controlled study targeting only fructans and galacto-oligosaccharides in patients with IBS-D26 and in primary care IBS patients with IBD that followed a low-FODMAP diet in combination with dietary advice from the NICE/BDA guidelines for IBS27. Recognizing avoidant/restrictive food intake disorder in IBS is essential to ensure that dietary management improves symptoms without causing nutritional, psychological, or social harm.

Adaptation of the FODMAP diet in people with IBS.
Source: Sanna Nybacka’s talk at IBS Days 2026.

 

Growing evidence suggests a role for functional foods, nutraceuticals, and herbal remedies, given their ability to target IBS pathophysiological mechanisms (gut motility, gut microbiome, gut barrier, immune function, and visceral sensitivity) with favorable profiles28. There are four levels of gut microbiome manipulation in IBS:

  1. Microbiome modulation with gut-directed antibiotics. Low FODMAP diet and rifaximin are equally effective for IBS-D29. However, current guidelines claim to limit the unnecessary use of rifaximin in IBS patients; biomarker-based strategies to enrich the likelihood of response to antibiotics in patients with IBS need to be identified.
  2. Microbiome supplementation with selected probiotics. Although efficacy appears to be strain-specific and results across studies are heterogeneous, selected probiotics have demonstrated beneficial effects on abdominal pain, bloating, and overall symptom burden in patients with IBS30,31. While the British Society of Gastroenterology, the World Gastroenterology Organization, and the more recent Italian guidelines consider probiotics a therapeutic option for global IBS symptoms, albeit with weak recommendations and low-quality evidence, the American College of Gastroenterology and the American Gastroenterological Association do not currently recommend their routine use because of insufficient and heterogeneous evidence.
  3. Postbiotic and purified microbial metabolites administration. Butyric acid is the most extensively investigated microbial metabolite owing to its beneficial effects on epithelial barrier integrity, mucosal immune regulation, intestinal inflammation, and visceral sensitivity32. A recent meta-analysis showed that postbiotic interventions (ie, a preparation of inanimate microorganisms and/or their components that confers a health benefit on the host) significantly improve abdominal pain and overall IBS severity while maintaining a safety profile comparable to placebo33. However, current clinical guidelines do not recommend their use in the management of IBS.
  4. Microbiome replacement with fecal microbiome transplants. Randomized controlled trials evaluating FMT in IBS have yielded highly variable results, ranging from no efficacy to substantial, durable symptom improvement. The most recent meta-analysis concluded that FMT may reduce IBS symptoms at 12 weeks compared with placebo, but the evidence remains very uncertain due to considerable heterogeneity among studies, including differences in study design, FMT protocols, donor selection, and diagnostic criteria34. Subgroup analyses reported symptom improvement when FMT was administered as a single dose and when IBS was diagnosed according to Rome IV criteria34.

Different levels of gut microbiome modulation in IBS.
Source: Carmelo Scarpignato’s talk at IBS Days 2026.

Predictors of response to gut microbiome modulation could help reduce the high variability currently seen in the efficacy of microbiome-targeted treatments. Baseline microbiota composition and functional capacity have consistently emerged as key predictors of therapeutic outcomes. For instance, patients with metabolic syndrome who have lower initial fecal microbiota alpha-diversity and lower abundance of Ruminococcus torques, a bacterium linked to poorer intestinal health and altered metabolite production, are more likely to benefit from lean donor FMT35.

Host-related factors—including immune status, disease phenotype, metabolic profile, medication exposure (e.g., history of systemic antibiotics), and dietary habits (e.g., daily intake of low-fermentable fiber36)—also contribute substantially to interindividual variability. Untargeted FMT has been shown to be effective in restoring decreased alpha diversity, reducing the persistence of proinflammatory taxa, and increasing beneficial taxa in diseases with acute dysbiosis (e.g., Clostridioides difficile infection, acute graft-versus-host disease, and immune checkpoint inhibitor-induced colitis). In contrast, FMT is less or not effective in non-infectious diseases with chronic/complex dysbiosis (e.g., IBS). While not all patients need microbiome modulation, we can identify those who do so through microbiome profiling or even clinical assessment. The integration of microbial and host-derived data is fostering the development of predictive models that can stratify patients and guide personalized therapeutic strategies.

The super-donor phenomenon in fecal microbiota transplantation in IBS and ulcerative colitis.
Source: Gianluca Ianiro’s talk at IBS Days 2026.

 

The future management of IBS will likely require a more personalized and integrative therapeutic model that balances robust evidence from traditional treatments with emerging data on microbiome-targeted interventions, while considering individual symptom patterns, microbiota signatures, dietary habits, and patient preferences.

The paradigm shift in IBS diagnosis and management is moving from symptom-based classification to biologically based, actionable endophenotypes.
Source: Javier Santos’ talk at IBS Days 2026.

 

Abstracts (63 were presented) featured at the meeting included, among others, subtype-specific epithelial alterations in IBS, AI-driven social listening research on the quality of nutrition information for improving gut health and patient-reported outcomes, the impact of sub-diagnostic bowel symptoms in the general population, and virtual reality-supported psychotherapy for the treatment of IBS.

The next IBS Days edition is scheduled for 2028.

 

References:

  1. Ma C, Ford AC, Hashash JG, et al. Recommendations for the evaluation and management of inflammatory bowel disease with irritable bowel syndrome-like symptoms: a joint Rome Foundation and International Organization for the Study of IBD (IOIBD) Consensus. Gastroenterology. 2026. doi: 10.1053/j.gastro.2026.04.008.
  2. Sperber AD, Freud T, Aziz I, et al. Greater overlap of Rome IV disorders of gut-brain interaction leads to increased disease severity and poorer quality of life. Clin Gastroenterol Hepatol. 2022; 20(5):e945-e956. doi: 10.1016/j.cgh.2021.05.042.
  3. Nabi MY, Nauhria S, Reel M, et al. Endometriosis and irritable bowel syndrome: A systematic review and meta-analyses. Front Med. 2022; 9:914356. doi: 10.3389/fmed.2022.914356.
  4. Shin A, Xu H, Sarnoff R, et al. Research communication: An observational cohort study on risk of ovarian cancer in women with irritable bowel syndrome. Aliment Pharmacol Ther. 2025; 62(9):944-947. doi: 10.1111/apt.70277.
  5. National Institute for Health and Care Excellence. Ovarian cancer: recognition and initial management. Last updated: 15 April 2026. Available: https://www.nice.org.uk/guidance/cg122/ifp/chapter/what-should-happen-when-you-see-your-gp
  6. Camilleri M, Carlson P, BouSaba J, et al. Comparison of biochemical, microbial and mucosal mRNA expression in bile acid diarrhoea and irritable bowel syndrome with diarrhoea. Gut. 2023; 72(1):54-65. doi: 10.1136/gutjnl-2022-327471.
  7. Zhan K, Zheng H, Li J, et al. Gut microbiota-bile acid crosstalk in diarrhea-irritable bowel syndrome. Biomed Res Int. 2020; 2020:3828249. doi: 10.1155/2020/3828249.
  8. Hanning N, Edwinson AL, Ceuleers H, et al. Intestinal barrier dysfunction in irritable bowel syndrome: a systematic review. Ther Adv Gastroenterol. 2021; 14:1756284821993586.
  9. Barbaro MR, Cremon C, Marasco G, et al. Molecular mechanisms underlying loss of vascular and epithelial integrity in irritable bowel syndrome. Gastroenterology. 2024; 167(6):1152-1166. doi: 10.1053/j.gastro.2024.07.004.
  10. Carloni S, Bertocchi A, Mancinelli S, et al. Identification of a choroid plexus vascular barrier closing during intestinal inflammation. Science. 2021; 374(6566):439-448. doi: 10.1126/science.abc6108.
  11. Britton TA, Grover M. Barrier restoration as a therapeutic strategy for disorders of gut-brain interaction. Lancet Gastroenterol Hepatol. 2026. doi: 10.1016/S2468-1253(26)00081-6. Published online.
  12. Gao J, Lee AA, Abtahi S, et al. Low fermentable oligosaccharides, disaccharides, monosaccharides, and polyols diet improves colonic barrier function and mast cell activation in patients with diarrhea-predominant irritable bowel syndrome. Gastroenterology. 2026; 170(1):132-147. doi: 10.1053/j.gastro.2025.07.016.
  13. Gąsiorowska A, Romanowski M, Walecka-Kapica E, et al. Efficacy and safety of a mixture of microencapsulated sodium butyrate, probiotics, and short chain fructooligosaccharides in patients with irritable bowel syndrome – a randomized, double-blind, placebo-controlled study. J Clin Med. 2024; 14(1):6. doi: 10.3390/jcm14010006.
  14. Zhou QQ, Verne ML, Fields JZ, et al. Randomised placebo-controlled trial of dietary glutamine supplements for postinfectious irritable bowel syndrome. Gut. 2019; 68(6):996-1002. doi: 10.1136/gutjnl-2017-315136.
  15. Inczefi O, Eutamene H, Placide F, et al. Translational evaluation of Gelsectan® effects on gut barrier dysfunction and visceral pain in animal models and irritable bowel syndrome with diarrhoea. United European Gastroenterol J. 2024; 12(8): 1102-1113. doi: 10.1002/ueg2.12625.
  16. Barbaro MR, Bianco F, Cremon C, et al. A probiotic mixture of Lactobacillus rhamnosus LR 32, Bifidobacterium lactis BL 04, and Bifidobacterium longum BB 536 counteracts the increase in permeability induced by the mucosal mediators of irritable bowel syndrome by acting on zonula occludens 1. Int J Mol Sci. 2025; 26(6):2656. doi: 10.3390/ijms26062656.
  17. Otte JM, Podolsky DK. Functional modulation of enterocytes by gram-positive and gram-negative microorganisms. Am J Physiol Gastrointest Liver Physiol. 2004; 286(4):G613-26. doi: 10.1152/ajpgi.00341.2003.
  18. Naso AM, Lizier M, Correale C, et al. A multi-strain probiotic formulation preserves intestinal epithelial and vascular barriers during enteropathogenic infection. Front Microbiol. 2025; 16:1631322. doi: 10.3389/fmicb.2025.1631322.
  19. Gong T, Chen Q, Mao H, et al. Outer membrane vesicles of Porphyromonas gingivalis trigger NLRP3 inflammasome and induce neuroinflammation, tau phosphorylation, and memory dysfunction in mice. Front Cell Infect Microbiol. 2022; 1 2:925435. doi: 10.3389/fcimb.2022.925435.
  20. Al-Nedawi K, Mian MF, Hossain N, et al. Gut commensal microvesicles reproduce parent bacterial signals to host immune and enteric nervous systems. FASEB J. 2015; 29(2):684-695. doi: 10.1096/fj.14-259721.
  21. Bayoumy AB, Mulder CJJ, Mol JJ, et al. Gut fermentation syndrome: A systematic review of case reports. United European Gastroenterol J. 2021; 9(3):332-243. doi: 10.1002/ueg2.12062.
  22. Vandekerckhove E, Janssens F, Tate D, et al. Treatment of gut fermentation syndrome with fecal microbiota transplantation. Ann Intern Med. 2020; 173(10):855. doi: 10.7326/L20-0341.
  23. Bamidele JO, Brownlow GM, Flack RM, et al. The Mediterranean diet for irritable bowel syndrome: a randomized clinical trial. Ann Intern Med. 2025; 178(12):1709-1717. doi: 10.7326/ANALS-25-01519.
  24. Singh P, Dean G, Iram S, et al. Efficacy of Mediterranean diet vs. low-FODMAP diet in patients with nonconstipated irritable bowel syndrome: a pilot randomized controlled trial. Neurogastroenterol Motil. 2025; 37(10):e70060. doi: 10.1111/nmo.70060.
  25. Staudacher HM, Mahoney S, Canale K, et al. Clinical trial: A Mediterranean diet is feasible and improves gastrointestinal and psychological symptoms in irritable bowel syndrome. Aliment Pharmacol Ther. 2024; 59(4):492-503. doi: 10.1111/apt.17791.
  26. Singh P, Chey SW, Nee J, et al. Is a simplified, less restrictive low FODMAP diet possible? Results from a double-blind, pilot randomized controlled trial. Clin Gastroenterol Hepatol. 2025; 23(2):362-364. doi: 10.1016/j.cgh.2024.04.021.
  27. Carbone F, Van den Houte K, Besard L, et al. Diet or medication in primary care patients with IBS: the DOMINO study – a randomised trial supported by the Belgian Health Care Knowledge Centre (KCE Trials Programme) and the Rome Foundation Research Institute. Gut. 2022; 71(11):2226-2232. doi: 10.1136/gutjnl-2021-325821.
  28. Marasco G, Cremon C, Salvi D, et al. Functional foods and nutraceuticals in irritable bowel syndrome. J Clin Med. 2025; 14(6):1830. doi: 10.3390/jcm14061830.
  29. Lee AA, Rao K, Singh P, et al. A randomized trial of rifaximin vs low fermentable oligosaccharides, disaccharides, monosaccharides, and polyols diet for symptom outcomes and microbiome changes in irritable bowel syndrome. Clin Gastroenterol Hepatol. 2026. doi: 10.1016/j.cgh.2026.04.014.
  30. Van der Geest AM, Schukking I, Brummer RJM, et al. Comparing probiotic and drug interventions in irritable bowel syndrome: a meta-analysis of randomised controlled trials. Benef Microbes. 2022; 13(3):183-194. doi: 10.3920/BM2021.0123.
  31. Goodoory VC, Khasawneh M, Black CJ, et al. Efficacy of probiotics in irritable bowel syndrome: systematic review and meta-analysis. Gastroenterology. 2022; 165(5):1206-1218. doi: 10.1053/j.gastro.2023.07.018.
  32. Caban M, Pikus E, Czarnecka-Chrebelska K, et al. Use of sodium butyrate and its microencapsulated forms in intestinal diseases-current clinical approach. Dig Dis Sci. 2026; 71(5):1626-1639. doi: 10.1007/s10620-025-09536-4.
  33. Ayad ME, Yu S, El Shennawy S, et al. Efficacy and safety of postbiotics in irritable bowel syndrome: a systematic review and meta-analysis. J Gastroenterol Hepatol. 2026; 41(7):1994-2005. doi: 10.1111/jgh.70421.
  34. Aumpan N, Watanabe J, Yuan Y, et al. Fecal microbiota transplantation for symptom improvement in patients with irritable bowel syndrome: systematic review and meta-analysis of randomized controlled trials. Gastroenterology. 2026. doi: 10.1053/j.gastro.2026.04.039.
  35. Kootte RS, Levin E, Salojärvi J, et al. Improvement of insulin sensitivity after lean donor feces in metabolic syndrome is driven by baseline intestinal microbiota composition. Cell Metab. 2017; 26(4):611-619. doi: 10.1016/j.cmet.2017.09.008.
  36. Mocanu V, Zhang Z, Deehan EC, et al. Fecal microbial transplantation and fiber supplementation in patients with severe obesity and metabolic syndrome: a randomized double-blind, placebo-controlled phase 2 trial. Nat Med. 2021; 27(7):1272-1279. doi: 10.1038/s41591-021-01399-2.