• dysbiosis
• female reproductive tract
• host‐microbiome interactions
• intestine
• oral
• skin
• tissue models

• 2337322 National Science Foundation CAREER Award
• R03DE030224 NIDCR NIH HHS

• dysbiosis
• fecal microbiota transplantation
• inflammatory bowel diseases
• microbiota

• complex human diseases
• disease similarity
• meta-analysis
• microbiome

• Humans
• Gastrointestinal Microbiome/genetics
• Diabetes Mellitus, Type 2/microbiology
• Machine Learning
• Crohn Disease/microbiology
• Colorectal Neoplasms/microbiology
• Metagenomics/methods
• Colitis, Ulcerative/microbiology
• Parkinson Disease/microbiology
• Schizophrenia/microbiology
• Alzheimer Disease/microbiology

• R01 AI130945 NIAID NIH HHS

• ulcerative colitis
• microbiome

• Humans
• Colitis, Ulcerative/microbiology
• Colitis, Ulcerative/therapy
• Colitis, Ulcerative/metabolism
• Fecal Microbiota Transplantation
• Male
• Female
• Feces/microbiology
• Bacteroides/genetics
• Adult
• Intestinal Mucosa/microbiology
• Intestinal Mucosa/metabolism
• Middle Aged
• Gastrointestinal Microbiome
• Treatment Failure
• RNA, Ribosomal, 16S/genetics
• Metabolome

• K12 GM081266-11 NIGMS NIH HHS
• T32 DK007007 NIDDK NIH HHS
• 1563159 National Science Foundation
• T32 DK007762 NIDDK NIH HHS
• K12 GM081266 NIGMS NIH HHS
• National Institute of Diabetes and Digestive and Kidney Diseases
• National Institute of General Medical Sciences
• Chan Zuckerberg Biohub
• Gladstone Institutes
• Kenneth Rainin Foundation
• Crohn’s and Colitis Foundation

• complex human diseases
• disease similarity
• meta-analysis
• microbiome

• R01 AI130945 NIAID NIH HHS

• Crohn’s Disease
• Inflammatory Bowel Disease
• Pathobionts
• Ulcerative Colitis

• Humans
• Inflammatory Bowel Diseases/therapy
• Inflammatory Bowel Diseases/microbiology
• Colitis, Ulcerative/drug therapy
• Crohn Disease/drug therapy
• Intestines
• Feces

• gut microbiota
• inflammatory bowel disease
• melatonin
• metabolism
• neurodegenerative disorders
• obesity
• sleep

• CB16/10/00239 Ministry of Economy and Competitiveness
• CB16/10/00239 Instituto de Salud Carlos III
• MCIN/AEI /10.13039/501100011033 / FEDER, UE Ministry of Science and Innovation

• colon targeting
• inflammatory bowel diseases
• microbiota
• natural polysaccharides
• oral delivery

• Crohn’s disease
• Dysbiosis
• Inflammation
• Microbiota
• Pouchitis
• Ulcerative colitis

• Humans
• Prebiotics
• Synbiotics
• Inflammatory Bowel Diseases/drug therapy
• Inflammatory Bowel Diseases/microbiology
• Probiotics/therapeutic use
• Microbiota
• Inflammation

• IBD
• microbiota
• n − 6
• prebiotic
• probiotic

• Humans
• Inflammatory Bowel Diseases
• Dysbiosis/therapy
• Microbiota
• Colitis, Ulcerative/pathology
• Inflammation

Inborn errors of immunity (IEI) are characterized by diverse clinical manifestations that are dominated by atypical, recurrent, chronic, or severe infectious or non-infectious features, including autoimmunity, lymphoproliferative disease, granulomas, and/or malignancy, which contribute substantially to morbidity and mortality. Some data suggest a correlation between clinical manifestations of IEI and altered gut microbiota. Many IEI display microbial dysbiosis resulting from the proliferation of pro-inflammatory bacteria or a decrease in anti-inflammatory bacteria with variations in the composition and function of numerous microbiota. Dysbiosis is considered more established, mainly within common variable immunodeficiency, selective immunoglobulin A deficiency, severe combined immunodeficiency diseases, Wiskott–Aldrich syndrome, Hyper-IgE syndrome, autoimmune polyendocrinopathy–candidiasis–ectodermal-dystrophy (APECED), immune dysregulation, polyendocrinopathy, enteropathy X-linked (IPEX) syndrome, IL-10 receptor deficiency, chronic granulomatous disease, and Kostmann disease. For certain IEIs, the specific predominance of gastrointestinal, respiratory, and cutaneous involvement, which is frequently associated with dysbiosis, justifies the interest for microbiome identification. With the better understanding of the relationship between gut microbiota, host immunity, and infectious diseases, the integration of microbiota modulation as a therapeutic approach or a preventive measure of infection becomes increasingly relevant. Thus, a promising strategy is to develop optimized prebiotics, probiotics, postbiotics, and fecal microbial transplantation to rebalance the intestinal microbiota and thereby attenuate the disease activity of many IEIs.

• Dysbiosis
• Gastrointestinal Microbiome
• Humans
• Immune System Diseases/genetics
• Immune System Diseases/microbiology
• Immunoglobulin A
• Receptors, Interleukin-10

• body niches
• dysbiosis
• evolution
• human microbiome
• restoration

• U54 MD007600 NIMHD NIH HHS
• P20 GM103475 NIGMS NIH HHS
• U54 CA096297 NCI NIH HHS
• R25 GM061838 NIGMS NIH HHS
• U54 MD007587 NIMHD NIH HHS
• S21 MD001830 NIMHD NIH HHS
• R25 GM061151 NIGMS NIH HHS

Salmonella enterica serovar Typhimurium (S. Typhimurium) is one of the common causes of human colitis. In the present study, two lytic phages vB_SenS-EnJE1 and vB_SenS-EnJE6 were isolated and the therapeutic effect of the combination of phages and faecal microbiota transplantation (FMT) on S. Typhimurium-induced mouse colitis was investigated. The characteristics and genome analysis indicated that they are suitable phages for phage therapy. Results showed that vB_SenS-EnJE1 lysis 41/54 Salmonella strains of serotype O4, and vB_SenS-EnJE6 lysis 46/54 Salmonella strains of serotypes O4 and O9. Severe inflammatory symptoms and disruption of the intestinal barrier were observed in S. Typhimurium -induced colitis. Interestingly, compared with a single phage cocktail (Pc) or single FMT, the combination of Pc and FMT (PcFMT) completely removed S. Typhimurium after 72 h of treatment, and significantly improved pathological damage and restored the intestinal barrier. Furthermore, PcFMT effectively restored the intestinal microbial diversity, especially for Firmicutes/Bacteroidetes [predominantly bacterial phyla responsible for the production of short-chain fatty acids (SCFA)]. Additionally, we found that PcFMT treatment significantly increased the levels of SCFA. All these data indicated that the combination of phages and FMT possesses excellent therapeutic effects on S. Typhimurium -induced intestinal microbiota disorder diseases. Pc and FMT played roles in “eliminating pathogens” and “strengthening vital qi,” respectively. This study provides a new idea for the treatment of intestinal microbiota disorder diseases caused by specific bacterial infections.

• National Natural Science Foundation of China

The human intestine harbors a huge number of diverse microorganisms where a variety of complex interactions take place between the microbes as well as the host and gut microbiota. Significant long-term variations in the gut microbiota (dysbiosis) have been associated with a variety of health conditions including inflammatory bowel disease (IBD). Conventional fecal microbiota transplantations (FMTs) have been utilized to treat IBD and have been proved promising. However, various limitations such as transient results, pathogen transfer, storage, and reproducibility render conventional FMT less safe and less sustainable. Defined synthetic microbial communities (SynCom) have been used to dissect the host-microbiota-associated functions using gnotobiotic animals or in vitro cell models. This review focuses on the potential use of SynCom in IBD and its advantages and relative safety over conventional FMT. Additionally, this review reinforces how various technological advances could be combined with SynCom to have a better understanding of the complex microbial interactions in various gut inflammatory diseases including IBD. Some technological advances including the availability of a gut-on-a-chip system, intestinal organoids, ex vivo intestinal cultures, AI-based refining of the microbiome structural and functional data, and multiomic approaches may help in making more practical in vitro models of the human host. Additionally, an increase in the cultured diversity from gut microbiota and the availability of their genomic information would further make the design and utilization of SynCom more feasible. Taken together, the combined use of the available knowledge of the gut microbiota in health and disease and recent technological advances and the development of defined SynCom seem to be a promising, safe, and sustainable alternative to conventional FMT in treating IBD.

• Dysbiosis
• Microbiome transplantation
• Microbiota

• Inflammatory bowel disease
• anti-inflammatory
• gut microbiota
• intestinal barrier function
• murine colitis models
• polysaccharides

• Humans
• Animals
• Mice
• Colitis/drug therapy
• Inflammatory Bowel Diseases/drug therapy
• Polysaccharides/pharmacology
• Polysaccharides/therapeutic use
• Anti-Inflammatory Agents/pharmacology
• Anti-Inflammatory Agents/therapeutic use
• Disease Models, Animal

Phosphodiesterase-4 (PDE4) functions as a catalyzing enzyme targeting hydrolyzation of intracellular cyclic adenosine monophosphate (cAMP) and inhibition of PDE4 has been proven to be a competitive strategy for dermatological and pulmonary inflammation. However, the pathological role of PDE4 and the therapeutic feasibility of PDE4 inhibitors in chronic ulcerative colitis (UC) are less clearly understood. This study introduced apremilast, a breakthrough in discovery of PDE4 inhibitors, to explore the therapeutic capacity in dextran sulfate sodium (DSS)-induced experimental murine chronic UC. In the inflamed tissues, overexpression of PDE4 isoforms and defective cAMP-mediating pathway were firstly identified in chronic UC patients. Therapeutically, inhibition of PDE4 by apremilast modulated cAMP-predominant protein kinase A (PKA)–cAMP-response element binding protein (CREB) signaling and ameliorated the clinical symptoms of chronic UC, as evidenced by improvements on mucosal ulcerations, tissue fibrosis, and inflammatory infiltrations. Consequently, apremilast maintained a normal intestinal physical and chemical barrier function and rebuilt the mucosal homeostasis by interfering with the cross-talk between human epithelial cells and immune cells. Furthermore, we found that apremilast could remap the landscape of gut microbiota and exert regulatory effects on antimicrobial responses and the function of mucus in the gut microenvironment. Taken together, the present study revealed that intervene of PDE4 provided an infusive therapeutic strategy for patients with chronic and relapsing UC.

• Epithelial barrier
• Gut microbiota
• Mucosal homeostasis
• PDE4
• Ulcerative colitis

The Qinghai-Tibet Plateau has a unique ecological environment, involving high altitude, low oxygen levels, strong ultraviolet rays, and severe imbalances in seasonal forage supply, which poses a serious threat to the livestock that feeds on natural pastures to maintain their survival. We have carried out a long-term follow-up study on rumen fermentation characteristics, the microbiota, and rumen epithelial gene expression of local Tibetan sheep. Correlation analysis showed that there were interactions among rumen fermentation characteristics, the microbiota, and host gene expression, mainly by adjusting the amino acid metabolism pathway and energy metabolism pathway to improve energy utilization. At the same time, we adjusted the balance of the rumen “core microbiota”, which was regulated to promote the development of rumen and maintain the homeostasis of rumen environment (which relies Tibetan sheep can better adapt to the harsh environment in different periods of the Qinghai-Tibet Plateau). This provides a theoretical basis for the breeding and management of Tibetan sheep on the Qinghai-Tibet Plateau.

As an important ruminant on the Qinghai-Tibet Plateau, Tibetan sheep can maintain their population reproduction rate in the harsh high-altitude environment of low temperature and low oxygen, which relies on their special plateau adaptations mechanism that they have formed for a long time. Microbiomes (known as “second genomes”) are closely related to the nutrient absorption, adaptability, and health of the host. In this study, rumen fermentation characteristics, the microbiota, and rumen epithelial gene expression of Tibetan sheep in various months were analyzed. The results show that the rumen fermentation characteristics of Tibetan sheep differed in different months. The total SCFAs (short-chain fatty acids), acetate, propionate, and butyrate concentrations were highest in October and lowest in June. The CL (cellulase) activity was highest in February, while the ACX (acid xylanase) activity was highest in April. In addition, the diversity and abundance of rumen microbes differed in different months. Bacteroidetes (53.4%) and Firmicutes (27.4%) were the dominant phyla. Prevotella_1 and Rikenellaceae_RC9_gut_group were the dominant genera. The abundance of Prevotella_1 was highest in June (27.8%) and lowest in December (17.8%). In addition, the expression of CLAUDIN4 (Claudin-4) and ZO1 (Zonula occludens 1) was significantly higher in April than in August and December, while the expression of SGLT1 (Sodium glucose linked transporter 1) was highest in August. Correlation analysis showed that there were interactions among rumen fermentation characteristics, the microbiota, and host gene expression, mainly by adjusting the amino acid metabolism pathway and energy metabolism pathway to improve energy utilization. At the same time, we adjusted the balance of the rumen “core microbiota” to promote the development of rumen and maintain the homeostasis of rumen environment, which makes Tibetan sheep better able to adapt to the harsh environment in different periods of the Qinghai-Tibet Plateau.

• 16S rRNA
• Tibetan sheep
• gene expression
• microbiota
• rumen fermentation

• Alzheimer's disease
• beta-amyloid
• central nervous system
• faecal microbiota transplantation
• gut microbiota
• probiotics

• colon
• inflammation
• melatonin
• microbiota dysfunction
• restraint stress

• Animals
• Antioxidants/pharmacology
• Bacteria
• Colon/microbiology
• Dysbiosis
• Gastrointestinal Microbiome/drug effects
• Inflammation
• Intestines
• Male
• Melatonin/pharmacology
• Mice
• NF-kappa B/metabolism
• Toll-Like Receptor 2/metabolism
• Toll-Like Receptor 4

The gut microbiome and the intestinal immune system are driving contributors to inflammatory bowel diseases (IBD). Both have an important signalling factor in common: short-chain fatty acids (SCFAs). SCFAs (acetate, propionate and butyrate) are produced by bacterial fermentation in the gut and exert several effects on host metabolism and immune system. This review provides an overview of the current knowledge of these effects, with specific focus on energy metabolism, intestinal barrier, immune system, and disease activity in IBD. To conclude, more research is needed on the cross-feeding mechanisms in the gut microbiome, as well as on the therapeutic potential of SCFAs on different disease models. Also randomized controlled trials and prospective cohort studies should investigate the clinical impact of SCFA administration.

• Acetate
• Butyrate
• Gut
• Inflammatory bowel disease
• Short chain fatty acids
• propionate

• Faecal microbiota transplantation
• donor effect
• inflammatory bowel disease
• super donor

• 16S rRNA profiling
• fecal microbiota transplantation
• microbiome
• ulcerative colitis

• antibiotic treatment
• fecal microbial transplantation
• inflammatory bowel disease

• fecal microbiota transplantation
• metabolites
• microbiota
• post-weaning diarrhea
• transcriptome

• immunity
• immunometabolism
• metabolism
• microbiota

• Colitis
• DSS
• GC
• Gut microbiota
• Inflammation

• Animals
• Colitis/prevention & control
• Colon/drug effects
• Colon/pathology
• Cytokines/metabolism
• Dextran Sulfate
• Disease Models, Animal
• Dose-Response Relationship, Drug
• Drugs, Chinese Herbal/administration & dosage
• Drugs, Chinese Herbal/pharmacology
• Gastrointestinal Microbiome/drug effects
• Inflammation/drug therapy
• Inflammation/pathology
• Male
• Mice
• Sulfasalazine/pharmacology

Fecal microbiota transplantation (FMT) is a promising strategy in the management of inflammatory bowel disease (IBD). The clinical effects of this practice are still largely unknown and unpredictable. In this study, two children affected by mild and moderate ulcerative colitis (UC), were pre- and post-FMT monitored for clinical conditions and gut bacterial ecology. Microbiota profiling relied on receipts’ time-point profiles, donors and control cohorts’ baseline descriptions. After FMT, the improvement of clinical conditions was recorded for both patients. After 12 months, the mild UC patient was in clinical remission, while the moderate UC patient, after 12 weeks, had a clinical worsening. Ecological analyses highlighted an increase in microbiota richness and phylogenetic distance after FMT. This increase was mainly due to Collinsella aerofaciens and Eubacterium biforme, inherited by respective donors. Moreover, a decrease of Proteus and Blautia producta, and the increment of Parabacteroides, Mogibacteriaceae, Bacteroides eggerthi, Bacteroides plebeius, Ruminococcus bromii, and BBacteroidesovatus were associated with remission of the patient’s condition. FMT results in a long-term response in mild UC, while in the moderate form there is probably need for multiple FMT administrations. FMT leads to a decrease in potential pathogens and an increase in microorganisms correlated to remission status.

• Pediatric Ulcerative Colitis (UC)
• fecal microbiota transplantation (FMT)
• gut bacterial ecology
• gut microbiota
• inflammatory bowel disease (IBD)

• Cohousing
• ConA hepatitis
• Coprophagy

• cardiovascular disease
• genetics
• inflammation
• microbial ecology
• periodontitis
• pleiotropy

We used a multi-omics profiling approach to investigate the suppressive effects of 2% Wolfberry (WOL)-enriched diets on dextran sodium sulfate (DSS)-induced colitis in mice. It was observed that in mice fed the WOL diet, the disease activity index, colon shortening, plasma concentrations of matrix metalloproteinase-3 and relative mesenteric fat weight were significantly improved as compared to the DSS group. Results from colon transcriptome and proteome profiles showed that WOL supplementation significantly ameliorated the expression of genes and proteins associated with the integrity of the colonic mucosal wall and colonic inflammation. Based on the hepatic transcriptome, proteome and metabolome data, genes involved in fatty acid metabolism, proteins involved in inflammation and metabolites related to glycolysis were downregulated in WOL mice, leading to lowered inflammation and changes in these molecules may have led to improvement in body weight loss. The integrated nutrigenomic approach thus revealed the molecular mechanisms underlying the ameliorative effect of whole WOL fruit consumption on inflammatory bowel disease.

• Inflammatory bowel disease
• Nutrition

• Administration, Oral
• Colitis, Ulcerative/therapy
• Combined Modality Therapy
• Fecal Microbiota Transplantation/methods
• Gastrointestinal Microbiome/drug effects
• Humans
• Probiotics/administration & dosage
• Probiotics/pharmacology
• Randomized Controlled Trials as Topic
• Treatment Outcome

• Jinan Science and Technology Bureau

• Crohn’s disease
• Fecal microbiota transplantation
• Randomized controlled trial

• Adrenal Cortex Hormones/therapeutic use
• Adult
• Crohn Disease/therapy
• Fecal Microbiota Transplantation
• Feces/microbiology
• Female
• Humans
• Male
• Microbiota
• Pilot Projects
• Remission Induction
• Research Design
• Severity of Illness Index
• Single-Blind Method
• Treatment Outcome

• Ministère de l’Enseignement Supérieur, de la Recherche Scientifique et des Technologies de l'Information et de la Communication
• Fondation de France
• Assistance Publique - Hôpitaux de Paris
• Association Francois Aupetit

Faecal microbiota transplantation (FMT) is a novel potential therapy for inflammatory bowel diseases, but it is poorly characterised.

We evaluated the performance of the mouse and rat as a pre-clinical model for human microbiota engraftment. We then characterised the effect of a single human stool transfer (HST) on a humanised model of DSS-induced colitis. Colonic and faecal microbial communities were analysed using the 16S rRNA approach and clinical manifestations were assessed in a longitudinal setting.

The microbial community of rats showed greater similarity to that of humans, while the microbiome of mice showed less similarity to that of humans. Moreover, rats captured more human microbial species than mice after a single HST. Using the rat model, we showed that HST compensated faecal dysbiosis by restoring alpha-diversity and by increasing the relative abundance of health-related microbial genera. To some extent, HST also modulated the microbial composition of colonic tissue. These faecal and colonic microbial communities alterations led to a relative restoration of colon length, and a significant decrease in both epithelium damage and disease severity. Remarkably, stopping inflammation by removing DSS before HST caused a faster and greater recovery of both microbiome and clinical manifestation features.

Our results indicate that the rat outperforms the mouse as a model for human microbiota engraftment and show that the efficacy of HST can be enhanced when inflammation stimulation is withdrawn. Finally, our findings support a new therapeutic strategy based on the use FMT combined with anti-inflammatory drugs.

• Faecal microbiota transplantation
• Inflammatory bowel disease
• Rat model of colitis

Antimicrobial peptides secreted by intestinal immune and epithelial cells are important effectors of innate immunity. They play an essential role in the maintenance of intestinal homeostasis by limiting microbial epithelium interactions and preventing unnecessary microbe‐driven inflammation. Pancreatitis‐associated protein (PAP) belongs to Regenerating islet‐derived III proteins family and is a C‐type (Ca⁺² dependent) lectin. PAP protein plays a protective effect presenting anti‐inflammatory properties able to reduce the severity of colitis, preserving gut barrier and epithelial inflammation. Here, we sought to determine whether PAP delivered at intestinal lumen by recombinant Lactococcus lactis strain (LL‐PAP) before and after chemically induced colitis is able to reduce the severity in two models of colitis. After construction and characterization of our recombinant strains, we tested their effects in dinitro‐benzenesulfonic‐acid (DNBS) and Dextran sulfate sodium (DSS) colitis model. After the DNBS challenge, mice treated with LL‐PAP presented less severe colitis compared with PBS and LL‐empty‐treated mice groups. After the DSS challenge, no protective effects of LL‐PAP could be detected. We determined that after 5 days administration, LL‐PAP increase butyrate producer's bacteria, especially Eubacterium plexicaudatum. Based on our findings, we hypothesize that a treatment with LL‐PAP shifts the microbiota preventing the severity of colon inflammation in DNBS colitis model. These protective roles of LL‐PAP in DNBS colitis model might be through intestinal microbiota modulation.

• SCFA
• SCFA-producing microbiota
• colonic immune
• gut microbiota

• Crohn’s disease
• adaptive/acquired immune system
• diet/nutrition
• dysbiosis/dysbacteriosis)
• environment
• ethnicity
• gastrointestinal disorders
• genetics
• indeterminate colitis
• inflammation
• inflammatory bowel disease
• innate immune system
• intestinal microbiota
• rural lifestyle
• ulcerative colitis
• urbanization

• UL1 TR000445 NCATS NIH HHS
• U54 CA091408 NCI NIH HHS
• U54 CA091405 NCI NIH HHS
• R21 DK095186 NIDDK NIH HHS
• UL1 RR024975 NCRR NIH HHS

We investigated the effects of early intervention with maternal fecal microbiota and antibiotics on gut microbiota and the metabolites. Five litters of healthy neonatal piglets (Duroc × Landrace × Yorkshire, nine piglets in each litter) were used. Piglets in each litter were orally treated with saline (CO), amoxicillin treatment (AM), or maternal fecal microbiota transplantation (MFMT) on days 1–6, with three piglets in each treatment. Results were compared to the CO group. MFMT decreased the relative abundances of Clostridium sensu stricto and Parabacteroides in the colon on day 7, whereas the abundance of Blautia increased, and the abundance of Corynebacterium in the stomach reduced on day 21. AM reduced the abundance of Arcanobacterium in the stomach on day 7 and reduced the abundances of Streptococcus and Lachnoclostridium in the ileum and colon on day 21, respectively. The metabolite profile indicated that MFMT markedly influenced carbohydrate metabolism and amino acid (AA) metabolism on day 7. On day 21, carbohydrate metabolism and AA metabolism were affected by AM. The results suggest that MFMT and AM discriminatively modulate gastrointestinal microflora and alter the colonic metabolic profiles of piglets and show different effects in the long-term. MFMT showed a location-specific influence on the gastrointestinal microbiota.

• early intervention
• fecal microbiota transplantation
• metabolite profiles
• neonatal pig

• Crohn's disease
• IBD
• Ulcerative colitis
• inflammation
• intestinal microbiology
• microbiome

• Acyl-Butyrolactones/chemistry
• Acyl-Butyrolactones/isolation & purification
• Acyl-Butyrolactones/metabolism
• Caco-2 Cells
• Cell Communication/genetics
• Epithelial Cells/metabolism
• Epithelial Cells/microbiology
• Escherichia coli/genetics
• Escherichia coli/isolation & purification
• Escherichia coli/metabolism
• Feces/microbiology
• Gastrointestinal Microbiome/genetics
• Gene Expression Regulation, Bacterial
• Humans
• Inflammatory Bowel Diseases/genetics
• Inflammatory Bowel Diseases/metabolism
• Inflammatory Bowel Diseases/microbiology
• Pseudomonas aeruginosa/genetics
• Pseudomonas aeruginosa/isolation & purification
• Quorum Sensing/genetics
• Signal Transduction

• Biocodex
• European Crohn's and Colitis Organization
• Association François Aupetit
• Fondation pour la Recherche Médicale
• Société nationale française de gastroentérologie