Pawel Kiela
University of Arizona, AZ·Microbiology & Immunology
Inflammatory bowel diseases (IBD), such as Crohn's disease and ulcerative colitis, cause chronic, relapsing inflammation of the gut. They involve a breakdown in the relationship between the body and its gut bacteria, but how the gut responds to shifting microbes remains poorly understood.
- Fields
Microbiology & Immunology
Physiology
Medicine & Clinical Research
- Topics
inflammatory bowel disease
colitis
Crohn's disease
- Grants
- 1 known grant, through Mar 2027
What they work on
- Determine whether loss of NAD+ or excess PARylation by the enzyme PARP1 is the main driver of experimental colitis, using PARP1 knockout mice and drug inhibition.
- Define how PARP1 and PARylation contribute to colitis caused by microbial communities from human IBD patients, transferred into germ-free mice.
- Work out how PARP1 in colon lining cells controls the interplay between gut microbiota, epithelial barrier function, and healing of the gut lining after injury, using epithelial-specific knockout mice.
- Examine how PARP1 shapes gut microbe composition and metabolism, and how it limits regulatory T cells (Tregs) in the inflamed colon.
More about the research
This project focuses on PARylation (poly-ADP-ribosylation), a chemical tag that enzymes attach to proteins. To build the tag, the enzymes consume NAD+, a key energy-related molecule. The team proposes that PARylation is a central driver of gut inflammation.
Why it matters
People with Crohn's disease or ulcerative colitis need new treatments. Because drugs that block PARP1 already exist and protected mice from gut injury, PARP1 activity could become a therapeutic target for IBD. Understanding how gut bacteria trigger excess PARylation may also point to new ways to restore a healthy gut lining.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Theresa Torres Pizarro
Case Western Reserve University, OH·Microbiology & Immunology
Identify the cell types in subepithelial ST2+ patches, cells that respond to the signaling molecule IL-33 and sit over colon polyps, in AOM/DSS-treated and Winnie mice, and test their function in tissue outside the body.
Joseph Lee
University of Colorado Denver/Anschutz Medical Campus, CO·Microbiology & Immunology·Early-career
Test whether the microbial purine hypoxanthine shapes the energy metabolism of gut lining cells by turning on TIGAR, a protein that reroutes sugar metabolism, and AMPK, a master energy sensor.
Sojin Shikano
University of Illinois Chicago, IL·Microbiology & Immunology
Characterize how strongly the TM4 peptide, a nanoparticle-forming copy of GPR15's fourth membrane-spanning segment, blocks GPR15L-triggered signaling through the GPR15 receptor in cell-based assays.
The school
University of Arizona: 36 labs on PI Pages, $1.0B a year on research, 487 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.