An observational study in Inflammatory Bowel Disease (Crohn's Disease and Ulcerative Colitis), Crohn Disease (CD) and Ulcerative Colitis (UC), sponsored by Seattle Children's Hospital. Recruiting at 1 site in United States. Open to participants aged 0 Years to 55 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2026-08-28.
Sponsored by Seattle Children's Hospital · Observational
Brief Summary
The aim of the FIBER study is to identify potential triggers associated with the later development of IBD (inflammatory bowel disease) based on baseline characteristics and biosamples (blood, urine, stool, saliva, and tissue).
Aim 1: To identify clinical, demographic, and immunologic factors associated with an increased risk of developing IBD in family members of IBD patients.
This aim will investigate the role of clinical factors (e.g., age of onset, gender, and family history), demographic factors (e.g., socioeconomic status, geographical location), and immune system markers (e.g., inflammatory cytokine profiles, immune cell populations) in predicting the likelihood of family members developing IBD over time.
Aim 2: To examine dietary, environmental, and immunologic influences on the development of IBD in family members of IBD patients.
This aim will explore how dietary habits (e.g., fiber, fats, processed foods), environmental exposures (e.g., smoking, pollution, and antibiotic use), and immune responses (e.g., changes in T-cell activation, inflammatory markers) contribute to the risk of IBD in family members.
Aim 3: To analyze the multi-omic (metagenomic, transcriptomic, proteomic) cellular signatures of host and microbial signatures in family members of IBD patients and their association with IBD onset.
This aim will investigate changes in the gut microbiome and immune-related gene expression profiles (transcriptomics) in family members. Specifically, the aim will focus on how shifts in microbial composition and host immune response genes (e.g., those involved in inflammation and epithelial barrier function) correlate with an increased risk of IBD development.
Aim 4: To investigate the multi-omic (metabolomic, transcriptomic, proteomic) cellular signature of host and microbial signatures in family members to identify biomarkers predictive of IBD development.
This aim will involve examining the metabolic, protein, and transcriptomic signatures (e.g., circulating cytokines, immune receptor expression) in blood, urine, or stool samples. The study will seek to identify early biomarkers from these profiles that can predict the onset of IBD, even in asymptomatic family members.
The familial nature of IBD has long been identified. Observational studies have highlighted a positive family history of IBD as a major risk factor for developing IBD, with particularly high risk among first-degree relatives (FDRs) of patients with Crohn's disease (CD). Importantly, an additive risk increment of CD onset appears with each additional affected FDR. Therefore, individuals within families with multiple affected members, also known as multiplex families, harbor notably high risk of developing CD. Healthy individuals from multiplex families have been shown to have a higher number of risk alleles in IBD-associated genes compared with healthy individuals from the general population, with the mean number of risk alleles increasing alongside increasing numbers of affected FDRs. However, none of the genetic markers could discriminate between individuals from single-case families (so-called simplex families) and individuals from multiplex families. Thus, genetics is unlikely to represent the sole factor explaining the increased risk, raising the question of factors driving the increased risk of CD in multiplex families.
As IBD involves pathological immune responses, detailed study of disease immunology is central to understanding pathogenesis and progression. Sc-RNAseq and other novel immunological techniques provide the capability to interrogate individual cellular transcripts to determine pathogenic pathways, even within rare cellular subpopulations previously inaccessible using conventional techniques and bulk RNA-seq. The novelty of single-cell technologies compared with previous technologies such as bulk sequencing lies in the ability to detect rare subsets of cells potentially representing aberrant drivers of disease. Available single-cell omic technologies are described in a research paper. The inherent advantage of single-cell techniques has led to continued popularity in IBD research 8-22.
Previous work from the research group has shown that sc-RNAseq can detect changes in pediatric IBD gut tissue from dissociated tissue biopsies. The proposed study will use immunological assays, including single-cell omics, to investigate risk factors associated with development of IBD among family members of patients with already diagnosed IBD.
1,550 studies on the registry are indexed under Inflammatory Bowel Diseases; 426 are open to participants now.
This study's planned enrollment of 7,000 is above the median of 140 across 626 observational studies indexed under Inflammatory Bowel Diseases.
Browse Inflammatory Bowel Diseases studies →Seattle Children's Hospital is the lead sponsor of 215 studies on the registry; 44 are open to participants now.
Counted across the registry records on this site, refreshed daily.
Asymptomatic first degree relative (FDR) (siblings or offspring) of patients with IBD aged between 0 and 55 years.
Go through the criteria one by one — yes, no or not sure — and take the list to your doctor or the study team. Kept in this browser only.
Exclusion Criteria:
Asymptomatic first degree relative (FDR) (siblings or offspring) of patients with CD aged between 0 and 55 years. Exclusion criteria for each subject population: * Nonviable neonates and uncertain viability neonates * Antibiotic treatment within 3 months prior to recruitment * Individuals with the presence of a known diagnosis of IBD, or symptoms suggestive of IBD * Not within the age range of 0-55 years
Serum antibody reactivity to microbial antigens measured using the Rapid Extracellular Antigen Profiling (REAP) assay, quantified as normalized REAP signal intensity (relative units) and assessed longitudinally.
Serum antibody reactivity to microbial antigens will be measured using the Rapid Extracellular Antigen Profiling (REAP) assay. Antigen-specific antibody reactivity will be quantified as normalized REAP signal intensity (relative units). REAP signal intensity will be compared between participants who subsequently develop IBD and participants who do not develop IBD during follow-up.
Time frame: Baseline, 6 months, 12 months, 18 months, 24 months, 30 months, 36 months, 42 months, 48 months, 54 months, 60 months, and at new IBD diagnosis.
Change in stool-based biomarkers associated with future IBD diagnosis
Time frame: Baseline, 6 months, 12 months, 18 months, 24 months, 30 months, 36 months, 42 months, 48 months, 54 months, 60 months, and at new IBD diagnosis.
Plan to share: No — IPD might not be shared since we do not have a plan yet.
No publications or documents are linked to this record.
Started Mar 2026 (actual). Primary completion is estimated for Feb 2036, 119 months after the start.
Of 243 non-industry observational studies under Inflammatory Bowel Diseases, half reached primary completion within 38 months of starting (the median), counting those still running; a quarter within 20 and three quarters within 132. This study's planned 119 months is above that.
Counting every sponsor, half of 280 studies reached it within 36 months; a quarter within 20 and three quarters within 122.
How these figures are worked out, and which studies are left out of them.
Eligibility is decided by the study team. Share this record with your doctor or contact the team directly.
Contact study teamGet an email when the registry record changes — status, dates, results — or when someone posts here.
Sign in to followQuestions and observations about this study, from anyone following it. Not medical advice, and not a channel to the study team — their contact details are on the registry record.
Sign in to join the discussion. Reading takes no account; posting does. You choose a display name, and a pseudonym is the default.
Nothing here yet. If you are running this trial, taking part in it, or weighing whether to, this is the place to say so.