Host-microbiota Interactions in Auto-inflammatory Diseases
ConditionAutoinflammatory Diseases
Trial statusRecruiting
Trial phaseNot listed
Trial typeObservational
Biological sexAll
Age12+
SponsorAssistance Publique - Hôpitaux de Paris
About this trial
Autoinflammatory diseases (AID) are genetic diseases responsible for excessive activation of innate immunity leading to blood inflammation and systemic symptoms. Most patients display digestive involvements that may resemble inflammatory bowel disease. Several studies have found dysbiosis in some AID. Gut microbiota can communicate with the host via gut-derived metabolites (Fatty acids, tryptophan, bile acids) that may have either pro-inflammatory or anti-inflammatory effects. Some metabolites can also activate the Aryl hydrocarbon receptor (AhR) pathway, which enhances gut barrier. Gut barrier dysfunction has already been associated with AID. Therfore, dysbiosis could promote digestive and inflammatory involvements in genetically predisposed patients via perturbations of gut-derived metabolites.
Eligibility criteria
This trial does not accept healthy volunteersQualifiers
Patients with autoinflammatory diseases aged >12 years and followed in the CEREMAIA internal medicine department present for consultation or day hospital for a routine care visit.
FMF defined by the Eurofever/PRINTO criteria
or CAPS définie by the Eurofever/PRINTO criteria
or MKD defined by the Eurofever/PRINTO criteria
Disqualifiers
Antibiotic therapy within 3 months prior to inclusion. If antibiotic therapy was initiated between inclusion and stool collection (data collected on the self-administered questionnaire accompanying the stool collection), the analysis data performed prior to antibiotic therapy will be retained, and the stool will not be analyzed.
Current infection on the day of inclusion
No social security
Refusal to participate
Trial population
Patients with auto-inflammatory diseases (Familial Mediterranean Fever, Mevalonate kinase deficiency, Cryopyrin-associated periodic fever, A20 haploinsufficiency, ADA2 deficiency, LACC1-associated juvenile arthritis, JAK1-associated autoinflammatory disease, or Syndrome of Undifferentiated Recurrent Fever ) followed up in the French reference center of autoinflammatory diseases.
Trial design
Design model
Case-control
Time perspective
Prospective
Treatments tested in this trial
Not listed
Trial groups
300 Participants
are grouped into 1 trial groupGroup A: Patients with autoinflammatory diseases
Trial outcomes
Primary outcomes
1
Stool and blood Gut-derived metabolites in patients with AID
Quantification of gut-derived metabolites in stools using mass spectrometry
Time frame
3 months2
Stool and blood Gut-derived metabolites in patients with AID
Qualitative evaluation of gut-derived metabolites in stools
Time frame
3 monthsSecondary outcomes
1
Role of AhR on activation of inflammatory pathways
Quantification of pro-inflammatory cytokines in presence of AhR agonists on patients' monocytes
Time frame
during the inclusion visit, baseline, day 12
Microbiota in AID patients
Dysbiosis measured by alpha and betadiversity
Time frame
3 months3
Effect of gut-derived metabolites on inflammatory pathways though cytokine production
Increase or decrease in proinflammatory cytokines secreted
Time frame
3 months4
Association of microbiota profile with biological control of the disease
Correlation between microbiota profiles and inflammation biomarkers (C-reactive protein, Serum A Amyloid, proteinuria)
Time frame
3 monthsSponsors and contacts
Click on the lead sponsor to view all of their trials.
Source ClinicalTrials.gov