Crohn DiseaseMESENCROHNNCT05891756
Mesenteric Bacterial Translocation in Evolved Crohn's Disease
An observational study of Crohn Disease, run by Hospital Mutua de Terrassa at 1 site in Spain.
Trial summary
Mesenteric fat can be invaded by gut bacteria through a process called bacterial translocation, which is the invasion of viable bacteria from the gastrointestinal tract to extraintestinal sites (mesenteric lymph nodes, liver, spleen, kidney, bloodstream, etc.). Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Crohn Disease
- How many people
- 40 participants
- Where
- 1 siteSpain
- Study dates
- 1 Jul 2022to Dec 2025
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Patients from the Hospital Universitari MútuaTerrassa
Who may be able to join
- Adults (18 years or older)
- Informed consent signed
- To require an ileocecal resection as part of the treatment of Crohn's Disease
- In the case of controls: not having Inflammatory Bowel Disease and requiring an ileocecal resection for another reason
Who cannot join
- To require an ileocecal resection with definitive or transient ileostomy
- In the case of controls: existence of a family history of Inflammatory Bowel Disease.
Trial locations and contacts
1 site in 1 country.
Yamile Zabana, MD, PhD contact
Spain1 site, 1 recruiting
- Recruiting
Hospital Universitari MútuaTerrassa
Terrassa, Barcelona, 08221
About this study
Mesenteric fat can be invaded by gut bacteria through a process called bacterial translocation, which is the invasion of viable bacteria from the gastrointestinal tract to extraintestinal sites (mesenteric lymph nodes, liver, spleen, kidney, bloodstream, etc.). In Crohn's disease (CD), bacterial translocation could increase the disproportionate inflammatory response already present and contribute to disease progression by stimulating the production of pro-inflammatory cytokines and immune-cell infiltration in the mesentery. Several mechanisms may promote bacterial translocation, such as bacterial overgrowth, disruption of the intestinal mucosal barrier and alterations in the immune system.
Ileocecal surgical resection is required in some patients with complicated or refractory CD. Unfortunately, post-surgical disease recurrence happens in up to 40% of cases, probably defining a subgroup of CD patients with a particular aggressive form of the disease. The complete microbiome (in gastrointestinal and extraintestinal sites) in CD patients that develop early post-surgical recurrence, as well as the association to innate immunity alterations, has not yet been studied.
Read more
The primary aim of the study is to explore the bacterial microbiome of CD patients and its association with early post-surgical recurrence and clinical or genetic variables related to innate immunity. To achieve this, the bacterial DNA present in mesenteric fat and ileal tissue (inflamed and non-inflamed) from surgical resection samples as well as blood samples from CD patients will be studied. Genetic polymorphisms, relevant clinical data and disease recurrence will also be evaluated.
The investigators hypothesize that bacterial translocation to the mesentery fat near the inflamed intestine is one of the mechanisms for perpetuation and chronicity of inflammation and therefore post-surgical recurrence in CD. The investigators expect to find a distinctive bacterial profile (in quantity and quality) in the mesenteric fat of patients with early post-surgical recurrence and/or with genetic variants that cause alterations in innate immunity.
The study of the microbiome in CD could help to identify the patients with a more aggressive disease form that will probably present early post-surgical recurrence, and could raise the possibility of microbial modulation as therapy for CD.
- Conditions
- Crohn Disease
- Keywords
- Crohn Disease, Mesenteric fat, Bacterial translocation, Innate immunity, Genetic polymorphisms
- Medical subject headings
- Crohn Disease
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| CD patients requiring surgical treatment (ileocecal resection) | Not described | |
| Control group | Patients requiring an ileocecal resection for a cause other than CD |
What is being measured
The primary outcome is the main question the study is designed to answer.
Differences in the proportions and abundance of bacterial taxa (defined as total percentage of bacterial DNA sequences) between the mesentery, ileal tissue and blood between CD patients with and without early post-surgical disease recurrence
Measured: at inclusion (surgery)
Differences in the function of the bacterial profile (defined as the metagenome function analysis) between the mesentery, ileal tissue and blood between CD patients with and without early post-surgical disease recurrence
Measured: at inclusion (surgery)
Secondary outcomes (1)
Association analysis of genetic variants related to innate immunity and the bacterial microbiome profile of CD patients
DNA polymorphisms detection in blood: ATG16L1 (rs2241880, rs3792109, rs3828309); NOD2 / CARD15 (rs2066844, rs2066845) and IRGM (rs13361189, rs4958847, rs1336119, rs10065172, rs7714584).
Measured: at inclusion (surgery)
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted7 Jun 2023
- Study start1 Jul 2022
- Primary completionJul 2024 (estimated)
- Study completionDec 2025 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (15)Papers the sponsor has linked to this study.
- Other trials for Crohn DiseaseStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case-control
- Time perspective
- Prospective
- Enrolment
- 40 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Hospital Mutua de Terrassa
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05891756
- Sponsor's protocol ID
- MESENCROHN
- Acronym
- MESENCROHN
- Status last verified
- Jun 2023
- First submitted
- 11 May 2023
- Last updated
- 22 Jun 2023
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Schaffler A, Scholmerich J. Innate immunity and adipose tissue biology. Trends Immunol. 2010 Jun;31(6):228-35. doi: 10.1016/j.it.2010.03.001.
PubMed 20434953Batra A, Heimesaat MM, Bereswill S, Fischer A, Glauben R, Kunkel D, Scheffold A, Erben U, Kuhl A, Loddenkemper C, Lehr HA, Schumann M, Schulzke JD, Zeitz M, Siegmund B. Mesenteric fat - control site for bacterial translocation in colitis? Mucosal Immunol. 2012 Sep;5(5):580-91. doi: 10.1038/mi.2012.33. Epub 2012 May 9.
PubMed 22569302Bertin B, Desreumaux P, Dubuquoy L. Obesity, visceral fat and Crohn's disease. Curr Opin Clin Nutr Metab Care. 2010 Sep;13(5):574-80. doi: 10.1097/MCO.0b013e32833cf0f4.
PubMed 20625283Alexander JW, Boyce ST, Babcock GF, Gianotti L, Peck MD, Dunn DL, Pyles T, Childress CP, Ash SK. The process of microbial translocation. Ann Surg. 1990 Oct;212(4):496-510; discussion 511-2. doi: 10.1097/00000658-199010000-00012.
PubMed 2222015Laffineur G, Lescut D, Vincent P, Quandalle P, Wurtz A, Colombel JF. [Bacterial translocation in Crohn disease]. Gastroenterol Clin Biol. 1992;16(10):777-81. French.
PubMed 1478405Zulian A, Cancello R, Micheletto G, Gentilini D, Gilardini L, Danelli P, Invitti C. Visceral adipocytes: old actors in obesity and new protagonists in Crohn's disease? Gut. 2012 Jan;61(1):86-94. doi: 10.1136/gutjnl-2011-300391. Epub 2011 Sep 19.
PubMed 21930728Shi H, Kokoeva MV, Inouye K, Tzameli I, Yin H, Flier JS. TLR4 links innate immunity and fatty acid-induced insulin resistance. J Clin Invest. 2006 Nov;116(11):3015-25. doi: 10.1172/JCI28898. Epub 2006 Oct 19.
PubMed 17053832Siegmund B. Mesenteric fat in Crohn's disease: the hot spot of inflammation? Gut. 2012 Jan;61(1):3-5. doi: 10.1136/gutjnl-2011-301354. Epub 2011 Nov 7. No abstract available.
PubMed 22068165Sokol H, Brot L, Stefanescu C, Auzolle C, Barnich N, Buisson A, Fumery M, Pariente B, Le Bourhis L, Treton X, Nancey S, Allez M, Seksik P; REMIND Study Group Investigators. Prominence of ileal mucosa-associated microbiota to predict postoperative endoscopic recurrence in Crohn's disease. Gut. 2020 Mar;69(3):462-472. doi: 10.1136/gutjnl-2019-318719. Epub 2019 May 29.
PubMed 31142586Domenech E, Manosa M, Bernal I, Garcia-Planella E, Cabre E, Pinol M, Lorenzo-Zuniga V, Boix J, Gassull MA. Impact of azathioprine on the prevention of postoperative Crohn's disease recurrence: results of a prospective, observational, long-term follow-up study. Inflamm Bowel Dis. 2008 Apr;14(4):508-13. doi: 10.1002/ibd.20359.
PubMed 18183602Gutierrez A, Scharl M, Sempere L, Holler E, Zapater P, Almenta I, Gonzalez-Navajas JM, Such J, Wiest R, Rogler G, Frances R. Genetic susceptibility to increased bacterial translocation influences the response to biological therapy in patients with Crohn's disease. Gut. 2014 Feb;63(2):272-80. doi: 10.1136/gutjnl-2012-303557. Epub 2013 Feb 1.
PubMed 23376290Li Y, Zuo L, Zhu W, Gong J, Zhang W, Gu L, Guo Z, Li N, Li J. The impact of bacterial DNA translocation on early postoperative outcomes in Crohn's patients undergoing abdominal surgery. J Crohns Colitis. 2015 Mar;9(3):259-65. doi: 10.1093/ecco-jcc/jju029. Epub 2015 Jan 2.
PubMed 25555386Takesue Y, Ohge H, Uemura K, Imamura Y, Murakami Y, Yokoyama T, Kakehashi M, Sueda T. Bacterial translocation in patients with Crohn's disease undergoing surgery. Dis Colon Rectum. 2002 Dec;45(12):1665-71. doi: 10.1007/s10350-004-7256-z.
PubMed 12473892Kosovac K, Brenmoehl J, Holler E, Falk W, Schoelmerich J, Hausmann M, Rogler G. Association of the NOD2 genotype with bacterial translocation via altered cell-cell contacts in Crohn's disease patients. Inflamm Bowel Dis. 2010 Aug;16(8):1311-21. doi: 10.1002/ibd.21223.
PubMed 20232407Kiernan MG, Coffey JC, McDermott K, Cotter PD, Cabrera-Rubio R, Kiely PA, Dunne CP. The Human Mesenteric Lymph Node Microbiome Differentiates Between Crohn's Disease and Ulcerative Colitis. J Crohns Colitis. 2019 Jan 1;13(1):58-66. doi: 10.1093/ecco-jcc/jjy136.
PubMed 30239655
Study at a glance
From the registry record, last updated by the sponsor on 22 Jun 2023. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Mesenteric Bacterial Translocation in Evolved Crohn's Disease
- ClinicalTrials.gov ID
- NCT05891756
- Acronym / sponsor ID
- MESENCROHN / MESENCROHN
- Conditions
- Crohn Disease
- Keywords
- Crohn Disease, Mesenteric fat, Bacterial translocation, Innate immunity, Genetic polymorphisms
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 40 participants (estimated)
- Lead sponsor
- Hospital Mutua de TerrassaUniversity, hospital or other
- Study start
- 1 Jul 2022 (actual)
- Primary completion
- Jul 2024 (estimated)
- Study completion
- Dec 2025 (estimated)
- First posted
- 7 Jun 2023 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Mesenteric fat can be invaded by gut bacteria through a process called bacterial translocation, which is the invasion of viable bacteria from the gastrointestinal tract to extraintestinal sites (mesenteric lymph nodes, liver, spleen, kidney, bloodstream, etc.). In Crohn's disease (CD), bacterial translocation could increase the disproportionate inflammatory response already present and contribute to disease progression by stimulating the production of pro-inflammatory cytokines and immune-cell infiltration in the mesentery. Several mechanisms may promote bacterial translocation, such as bacterial overgrowth, disruption of the intestinal mucosal barrier and alterations in the immune system.
Ileocecal surgical resection is required in some patients with complicated or refractory CD. Unfortunately, post-surgical disease recurrence happens in up to 40% of cases, probably defining a subgroup of CD patients with a particular aggressive form of the disease. The complete microbiome (in gastrointestinal and extraintestinal sites) in CD patients that develop early post-surgical recurrence, as well as the association to innate immunity alterations, has not yet been studied.
The primary aim of the study is to explore the bacterial microbiome of CD patients and its association with early post-surgical recurrence and clinical or genetic variables related to innate immunity. To achieve this, the bacterial DNA present in mesenteric fat and ileal tissue (inflamed and non-inflamed) from surgical resection samples as well as blood samples from CD patients will be studied. Genetic polymorphisms, relevant clinical data and disease recurrence will also be evaluated.
The investigators hypothesize that bacterial translocation to the mesentery fat near the inflamed intestine is one of the mechanisms for perpetuation and chronicity of inflammation and therefore post-surgical recurrence in CD. The investigators expect to find a distinctive bacterial profile (in quantity and quality) in the mesenteric fat of patients with early post-surgical recurrence and/or with genetic variants that cause alterations in innate immunity.
The study of the microbiome in CD could help to identify the patients with a more aggressive disease form that will probably present early post-surgical recurrence, and could raise the possibility of microbial modulation as therapy for CD.
Study design
- Observational model
- Case-control
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| CD patients requiring surgical treatment (ileocecal resection) | – | – |
| Control group | – | –Patients requiring an ileocecal resection for a cause other than CD |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Patients from the Hospital Universitari MútuaTerrassa
Key inclusion criteria (4 listed)
- Adults (18 years or older)
- Informed consent signed
- To require an ileocecal resection as part of the treatment of Crohn's Disease
- In the case of controls: not having Inflammatory Bowel Disease and requiring an ileocecal resection for another reason
Key exclusion criteria (2 listed)
- To require an ileocecal resection with definitive or transient ileostomy
- In the case of controls: existence of a family history of Inflammatory Bowel Disease.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Differences in the proportions and abundance of bacterial taxa (defined as total percentage of bacterial DNA sequences) between the mesentery, ileal tissue and blood between CD patients with and without early post-surgical disease recurrence
Time frame: at inclusion (surgery)
Differences in the function of the bacterial profile (defined as the metagenome function analysis) between the mesentery, ileal tissue and blood between CD patients with and without early post-surgical disease recurrence
Time frame: at inclusion (surgery)
1 secondary outcome
Association analysis of genetic variants related to innate immunity and the bacterial microbiome profile of CD patients
Time frame: at inclusion (surgery)
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 22 Jun 2023.
- Background: PubMed 20434953Schaffler A, Scholmerich J. Innate immunity and adipose tissue biology. Trends Immunol. 2010 Jun;31(6):228-35. doi: 10.1016/j.it.2010.03.001.
- Background: PubMed 22569302Batra A, Heimesaat MM, Bereswill S, Fischer A, Glauben R, Kunkel D, Scheffold A, Erben U, Kuhl A, Loddenkemper C, Lehr HA, Schumann M, Schulzke JD, Zeitz M, Siegmund B. Mesenteric fat - control site for bacterial translocation in colitis? Mucosal Immunol. 2012 Sep;5(5):580-91. doi: 10.1038/mi.2012.33. Epub 2012 May 9.
- Background: PubMed 20625283Bertin B, Desreumaux P, Dubuquoy L. Obesity, visceral fat and Crohn's disease. Curr Opin Clin Nutr Metab Care. 2010 Sep;13(5):574-80. doi: 10.1097/MCO.0b013e32833cf0f4.
- Background: PubMed 2222015Alexander JW, Boyce ST, Babcock GF, Gianotti L, Peck MD, Dunn DL, Pyles T, Childress CP, Ash SK. The process of microbial translocation. Ann Surg. 1990 Oct;212(4):496-510; discussion 511-2. doi: 10.1097/00000658-199010000-00012.
- Background: PubMed 1478405Laffineur G, Lescut D, Vincent P, Quandalle P, Wurtz A, Colombel JF. [Bacterial translocation in Crohn disease]. Gastroenterol Clin Biol. 1992;16(10):777-81. French.
- Background: PubMed 21930728Zulian A, Cancello R, Micheletto G, Gentilini D, Gilardini L, Danelli P, Invitti C. Visceral adipocytes: old actors in obesity and new protagonists in Crohn's disease? Gut. 2012 Jan;61(1):86-94. doi: 10.1136/gutjnl-2011-300391. Epub 2011 Sep 19.
- Background: PubMed 17053832Shi H, Kokoeva MV, Inouye K, Tzameli I, Yin H, Flier JS. TLR4 links innate immunity and fatty acid-induced insulin resistance. J Clin Invest. 2006 Nov;116(11):3015-25. doi: 10.1172/JCI28898. Epub 2006 Oct 19.
- Background: PubMed 22068165Siegmund B. Mesenteric fat in Crohn's disease: the hot spot of inflammation? Gut. 2012 Jan;61(1):3-5. doi: 10.1136/gutjnl-2011-301354. Epub 2011 Nov 7. No abstract available.
- Background: PubMed 31142586Sokol H, Brot L, Stefanescu C, Auzolle C, Barnich N, Buisson A, Fumery M, Pariente B, Le Bourhis L, Treton X, Nancey S, Allez M, Seksik P; REMIND Study Group Investigators. Prominence of ileal mucosa-associated microbiota to predict postoperative endoscopic recurrence in Crohn's disease. Gut. 2020 Mar;69(3):462-472. doi: 10.1136/gutjnl-2019-318719. Epub 2019 May 29.
- Background: PubMed 18183602Domenech E, Manosa M, Bernal I, Garcia-Planella E, Cabre E, Pinol M, Lorenzo-Zuniga V, Boix J, Gassull MA. Impact of azathioprine on the prevention of postoperative Crohn's disease recurrence: results of a prospective, observational, long-term follow-up study. Inflamm Bowel Dis. 2008 Apr;14(4):508-13. doi: 10.1002/ibd.20359.
- Background: PubMed 23376290Gutierrez A, Scharl M, Sempere L, Holler E, Zapater P, Almenta I, Gonzalez-Navajas JM, Such J, Wiest R, Rogler G, Frances R. Genetic susceptibility to increased bacterial translocation influences the response to biological therapy in patients with Crohn's disease. Gut. 2014 Feb;63(2):272-80. doi: 10.1136/gutjnl-2012-303557. Epub 2013 Feb 1.
- Background: PubMed 25555386Li Y, Zuo L, Zhu W, Gong J, Zhang W, Gu L, Guo Z, Li N, Li J. The impact of bacterial DNA translocation on early postoperative outcomes in Crohn's patients undergoing abdominal surgery. J Crohns Colitis. 2015 Mar;9(3):259-65. doi: 10.1093/ecco-jcc/jju029. Epub 2015 Jan 2.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Yamile Zabana, MD, PhD contact
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Crohn Disease, run by Hospital Mutua de Terrassa at 1 site in Spain.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 4 inclusion and 2 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 22 Jun 2023. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Spain. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Yamile Zabana, MD, PhD (yzabana@gmail.com), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Differences in the proportions and abundance of bacterial taxa (defined as total percentage of bacterial DNA sequences) between the mesentery, ileal tissue and blood between CD patients with and without early post-surgical disease recurrence (time frame: at inclusion (surgery)). The study lists 2 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT05891756, which also lists 15 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 22 Jun 2023.