Grant: Fellowship - Priority Announcement: Gastroenterology
University of British Columbia
$0.00
IL-37 recruitment of SIGIRR: A novel mechanism to suppress intestinal epithelial cell driven inflammation and microbial dysbiosis in Inflammatory Bowel Disease.
FY 2016-17
Summary
Patients with Inflammatory Bowel Disease (IBD) suffer bouts of extreme gut inflammation that disrupt the population of bacteria in their intestines. Thus IBD patients often have fewer beneficial bacteria and suffer an overgrowth of potentially dangerous bacteria. In healthy individuals, such responses are typically prevented by SIGIRR, a protein made by the cells that line the gut. SIGIRR acts by suppressing mechanisms that drive inflammation. We have shown that loss of SIGIRR dramatically increases inflammation and drives bacterial imbalance. The inflammation can become so severe that gut tissue can become necrotic. We do not have a way to promote the beneficial actions of SIGIRR in the gut, but recently, a newly recognized anti-inflammatory compound called interleukin (IL)-37, has been shown to interact with SIGIRR to inhibit inflammatory responses in human cells. In this project, we plan to test whether IL-37 stimulates SIGIRR to: i) control inflammation and suppress bacterial killing responses in the cells that line the gut; ii) protect mice from experimentally-induced IBD; and iii) promote normal gut microbe balance. Ultimately, my studies will explore the potential for IL-37 to act as a new therapeutic for patients with IBD.
Department
Program
Fellowship - Priority Announcement: Gastroenterology
Recipient
Location
British Columbia, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
363772
Name
Allaire Joannie
Region
British Columbia
Country
Canada
Orgtype
Institution Paid; Research Institution
Partnername
Canadian Association of Gastroenterology (Oakville, Ontario)
Instname2
Infection and Immunity
Theme2
Biomedical
Prcname2
Fellowships - Post-PhD
Projecttitle
IL-37 recruitment of SIGIRR: A novel mechanism to suppress intestinal epithelial cell driven inflammation and microbial dysbiosis in Inflammatory Bowel Disease.
Programtype2
Fellowship Programs
Orgnameinp2
University of British Columbia
Cihramount2
$0
Cihrequipment2
$0
Programname2
Fellowship - Priority Announcement: Gastroenterology
Keyworddelim
Dysbiosis; Enteroids; Epithelial Cells; Ibd; Il37; Innate Immune Signaling; Microbiota; Pathobionts; Sigirr
Abstract
Patients with Inflammatory Bowel Disease (IBD) suffer bouts of extreme gut inflammation that disrupt the population of bacteria in their intestines. Thus IBD patients often have fewer beneficial bacteria and suffer an overgrowth of potentially dangerous bacteria. In healthy individuals, such responses are typically prevented by SIGIRR, a protein made by the cells that line the gut. SIGIRR acts by suppressing mechanisms that drive inflammation. We have shown that loss of SIGIRR dramatically increases inflammation and drives bacterial imbalance. The inflammation can become so severe that gut tissue can become necrotic. We do not have a way to promote the beneficial actions of SIGIRR in the gut, but recently, a newly recognized anti-inflammatory compound called interleukin (IL)-37, has been shown to interact with SIGIRR to inhibit inflammatory responses in human cells. In this project, we plan to test whether IL-37 stimulates SIGIRR to: i) control inflammation and suppress bacterial killing responses in the cells that line the gut; ii) protect mice from experimentally-induced IBD; and iii) promote normal gut microbe balance. Ultimately, my studies will explore the potential for IL-37 to act as a new therapeutic for patients with IBD.
Competitiondate
201611
Approvedterm2
2 yrs 0 mth
Pinamesdelim
Allaire, Joannie
Approvedterm
2 ans 0 mois