Theresa Torres Pizarro
Case Western Reserve University, OH·Microbiology & Immunology
The lining of the gut acts as a barrier between the body and trillions of microbes. In inflammatory bowel disease (IBD), including ulcerative colitis, this barrier fails and the gut becomes chronically inflamed, and years of inflammation raise the risk of colorectal cancer.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Biochemistry
- Topics
inflammatory bowel disease
ulcerative colitis
colitis-associated cancer
- Grants
- 2 known grants, through Jun 2030
What they work on
- 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.
- Determine in living mice what role polyp-associated ST2+ cells play in colitis-associated cancer, and confirm their presence in polyps from patients.
- Test whether GSDMB isoforms, gene versions made by alternative splicing, differ between gut lining cells of IBD patients and controls, and how the rs11078926 variant changes them.
- Determine how S-nitrosylation, a chemical tag on cysteine, regulates GSDMB-driven wound healing in intestinal epithelial cells, including those carrying IBD-associated mutant GSDMB.
More about the research
Both projects ask how cells in the gut lining and the signals they respond to decide between healing, ongoing inflammation and cancer.
Why it matters
People with ulcerative colitis and other forms of IBD face lifelong symptoms and a higher risk of colorectal cancer, sometimes needing colon removal. The ST2-bearing cells over polyps could become markers for early detection or targets to prevent colitis-associated cancer. Knowing which GSDMB forms help or harm the gut lining could guide new drugs that restore barrier repair in IBD patients.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Pawel Kiela
University of Arizona, AZ·Microbiology & Immunology
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.
Philip Busbee
University of South Carolina-Columbia, SC·Microbiology & Immunology
Test whether eating microplastics of different sizes worsens depression-like behavior and markers of brain inflammation in mice with colitis induced by dextran sodium sulfate (DSS), a model of ulcerative colitis.
Ting Fu
University of Wisconsin-Madison, WI·Microbiology & Immunology
Determine how host- and microbe-derived bile acids generated during inflammation and tumor growth shape gut macrophages and their crosstalk with T cells and intestinal stem cells.
The school
Case Western Reserve University: 34 labs on PI Pages, $643M a year on research, 213 research doctorates a year.
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