Ignite Creation Date:
2025-12-24 @ 9:25 PM
Ignite Modification Date:
2025-12-30 @ 5:25 PM
Study NCT ID:
NCT01930032
Status:
COMPLETED
Last Update Posted:
2017-03-08
First Post:
2013-08-20
Is NOT Gene Therapy:
True
Has Adverse Events:
False
Brief Title:
Pathogenic Mechanisms in C Diff Infection and Colitis
Sponsor:
Beth Israel Deaconess Medical Center
Organization:
Study Overview
Official Title:
Pathogenic Mechanisms in Clostridium Difficile Infection and Colitis
Status:
COMPLETED
Status Verified Date:
2017-03
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
The purpose of this study is to learn more about infection by Clostridium difficile (also known as C. difficile). C. difficile is a common bacterium (a germ that may cause disease) that can live in the human gut. Some people have it without having any symptoms. In other people it can cause illness ranging from mild diarrhea to severe colitis (infection of the colon).
C. difficile makes toxins that damage the cells that line the colon. The study doctors want to find out how these toxins cause damage to the cells in the colon.
C. difficile makes toxins that damage the cells that line the colon. The study doctors want to find out how these toxins cause damage to the cells in the colon.
Detailed Description:
The purpose of this study is to examine pathogenic mechanisms of Clostridium difficile toxin-mediated intestinal injury and inflammation. Two primary mechanisms will be examined.
* To examine the hypothesis is that microRNA expression profiles are dysregulated by Clostridium difficile toxin exposure and that dysregulation of miRNA expression plays a role in the pathogenesis of C. difficile associated diseases.
* To examine the hypothesis is that the TLR9 receptor mediates key inflammatory events in response to Clostridium difficile toxin exposure.
* To examine the hypothesis is that microRNA expression profiles are dysregulated by Clostridium difficile toxin exposure and that dysregulation of miRNA expression plays a role in the pathogenesis of C. difficile associated diseases.
* To examine the hypothesis is that the TLR9 receptor mediates key inflammatory events in response to Clostridium difficile toxin exposure.
Study Oversight
Has Oversight DMC:
False
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?: