INF-α Innate Immune Response to Gliadin

Celiac Disease Clinical Trial

Official title:

A Gliadin Peptide Regulated the INF-α Immune Response in Celiac Small Intestine and in an En-terocyte Cell Line

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT03221647
• Other study ID #: Innate immunity CD
• Status: Completed
• Phase: N/A
• First received: July 7, 2017
• Last updated: July 17, 2017
• Start date: January 10, 2013
• Est. completion date: July 1, 2017

Study information

• Verified date: July 2017
• Source: Federico II University
• Contact: n/a
• Is FDA regulated: No
• Study type: Observational [Patient Registry]

Clinical Trial Summary

Background & Aims The enteropathy in Celiac Disease (CD) is due the adaptive and to the innate immune response to gliadin peptides. Gliadin peptide P31-43 activates innate immune response and interferes with vesicular trafficking. Type 1 interferons (INFs) and viral infections play a role in CD pathogenesis. In this paper investigators investigated the role of P31-43 in the activation of the INF-α pathway.

Methods Small intestinal biopsies of CD patients both with active disease on gluten containing diet (GCD) and in remission phase of the disease on a gluten free diet (GFD) and controls were analyzed before and after culture with P31-43. The levels of toll like receptor 7 (TLR7), myeloid differentiation primary response 88 (MyD88), myxovirus resistance protein 1 (MxA) and nuclear factor-κB (NF-κB) proteins and INF-α mRNA was analyzed in intestinal biopsies.

Description:

Intestinal biopsies from CD patients and controls were obtained after EGDS performed during routine analysis. The biopsies were immediately immersed in culture medium (Dulbecco's modified medium, DMEM) in a falcon tube and kept for 16h at 37 C before cultivation. Biopsies were cultivated as described in Barone MV1, Caputo I, Ribecco MT, Maglio M, Marzari R, Sblattero D, Troncone R, Auricchio S, Esposito C. Humoral immune response to tissue transglutaminase is related to epithelial cell proliferation in celiac disease. Gastroenterology. 2007,132(4):1245-53.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 53
• Est. completion date: July 1, 2017
• Est. primary completion date: July 1, 2017
• Gender: All
• Age group: 2 Years to 17 Years

Eligibility

Inclusion Criteria:

biopsy fragments from duodenum were obtained from CD patients with villous atrophy on GCD, controls, affected by gastroesophageal reflux, and CD patients on GFD.

Exclusion Criteria:

other inflammatory intestinal diseases

Related Conditions & MeSH terms

• Celiac Disease

Intervention

Other:
• Intestinal biopsies
Intestinal biopsies obtained from Patients and Controls by EGDS. The patients and controls had the intestinal biopsies as a diagnostic step or routine check independently from the present study. For this study 3 additional biopsies samples were done in patients and controls that signed the informed consent.

Locations

Country	Name	City	State
Italy	Riccardo Troncone	Naples

Sponsors (1)

Lead Sponsor	Collaborator
Federico II University

Country where clinical trial is conducted

Italy, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Measurement of Mxa and INF alpha proteins in CD biopsies compared to controls	Intestinal biopsies from CD patients and controls were used to study protein levels of MxA and INF-alpha by western blot. MxA protein levels were compared to tubulin and ERK as loading control. Student t test was used to analyse the data.	through study completion, an average of 1 year