The Innate Immune System and Inflammatory Bowel Disease

NCT00516776 | Completed

• 1 other identifier: 5.2007.910
• Study Type: observational
• Target: 400
• Locations: 1 country
• Sites: 1

Brief Summary

The study includes individuals with ulcerative colitis, Crohn's disease and healthy controls. The purpose of this study is to examine the innate immune system (IIS) by exposing peripheral blood monocytes to various ligands relevant for stimulation of the IIS and study the immune response. Colonic mucosal samples are examined to find gene expression patterns which may distinguish the two forms of disease from each other and from healthy controls. The hypothesis is that the innate immune system has responses unique for the disease states, and that the diseases may be differentiated by examination of gene expression patterns in mucosal biopsies.

Conditions

Ulcerative Colitis; Crohn's Disease

Outcome Measures

Primary Outcomes (1)

• gene expression patterns in mucosal biopsies

  2 years

Eligibility Criteria

• Age: 18 Years+
• Sex: all
• Healthy Volunteers: Yes
• Age Groups: Adult (18-64), Older Adult (65+)
• Sampling Method: Probability Sample

Study Population

Patients from endoscopy unit and outpatients clinic with ulcerative colitis, Crohn's disease and healthy controls

You may qualify if:

• Presence of ulcerative colitis
• Presence of Crohn's disease
• Healthy (no sign of inflammatory bowel disease)

You may not qualify if:

• Anticoagulation
• Cardiac valvular disease
• Intravascular prosthesis
• Coagulation disorders
• Gastrointestinal malignancy

Sponsors & Collaborators

• Norwegian University of Science and Technology: lead
• The Royal Norwegian Ministry of Health: collaborator

Study Sites (1)

Dept of Cancer Research and Molecular Medicine, NTNU

Trondheim, NO-7489, Norway

Location

Related Publications (3)

• Brenna O, Bruland T, Furnes MW, Granlund Av, Drozdov I, Emgard J, Bronstad G, Kidd M, Sandvik AK, Gustafsson BI. The guanylate cyclase-C signaling pathway is down-regulated in inflammatory bowel disease. Scand J Gastroenterol. 2015;50(10):1241-52. doi: 10.3109/00365521.2015.1038849. Epub 2015 May 15.

  PMID: 25979109 DERIVED

• Ostvik AE, Granlund Av, Gustafsson BI, Torp SH, Espevik T, Mollnes TE, Damas JK, Sandvik AK. Mucosal toll-like receptor 3-dependent synthesis of complement factor B and systemic complement activation in inflammatory bowel disease. Inflamm Bowel Dis. 2014 Jun;20(6):995-1003. doi: 10.1097/MIB.0000000000000035.

  PMID: 24739633 DERIVED

• Ostvik AE, Granlund AV, Bugge M, Nilsen NJ, Torp SH, Waldum HL, Damas JK, Espevik T, Sandvik AK. Enhanced expression of CXCL10 in inflammatory bowel disease: potential role of mucosal Toll-like receptor 3 stimulation. Inflamm Bowel Dis. 2013 Feb;19(2):265-74. doi: 10.1002/ibd.23034.

  PMID: 22685032 DERIVED

Biospecimen

Retention: SAMPLES WITH DNA

Intestinal biopsies Plasma/serum Peripheral blood monocytes

MeSH Terms

Conditions

Colitis, Ulcerative; Crohn Disease

Condition Hierarchy (Ancestors)

Colitis; Gastroenteritis; Gastrointestinal Diseases; Digestive System Diseases; Inflammatory Bowel Diseases; Colonic Diseases; Intestinal Diseases

Study Officials

• Arne K Sandvik, MD PhD

  Norwegian University of Science and Technology

  PRINCIPAL INVESTIGATOR

Study Design

• Study Type: observational
• Observational Model: CASE CONTROL
• Time Perspective: CROSS SECTIONAL
• Sponsor Type: OTHER
• Responsible Party: SPONSOR

Study Record Dates

• First Submitted: August 14, 2007
• First Posted: August 15, 2007
• Study Start: June 1, 2007
• Primary Completion: December 1, 2017
• Study Completion: December 1, 2017
• Last Updated: February 14, 2018

Record last verified: 2018-02

Data Sharing

• IPD Sharing: Will not share

Locations

NO (1)