Babajide Ojo
University of Alabama at Birmingham, AL·Medicine & Clinical Research·Early-career
Ulcerative colitis (UC), a chronic inflammatory disease of the colon, is becoming more common in children every year. The colon's inner lining is a protective barrier that is constantly renewed by stem cells, and those stem cells depend on healthy mitochondria, the cell's energy factories.
- Fields
Medicine & Clinical Research
Physiology
Biology
- Topics
ulcerative colitis
inflammatory bowel disease
pediatric gastroenterology
- Grants
- 1 known grant, through Jul 2028
What they work on
- Define how sulfites regulate mitochondrial metabolism and cell differentiation in colon organoids grown from healthy children and children with ulcerative colitis.
- Map sulfite-induced and sulfite-susceptible chromatin sites in pediatric colon tissue to explain sulfite-driven metabolic and differentiation defects.
- Test how sulfite exposure and loss of Mocs1, a gene needed for mitochondrial sulfite clearance, in the colon lining shape colon biology in physiologically relevant in vivo models.
More about the research
Colon tissue from children with UC shows clear mitochondrial damage. Because diet constantly affects the gut, this project asks whether sulfites harm mitochondria in the colon lining. Sulfites are compounds the body makes from sulfur-containing molecules, and they are also common food preservatives.
Why it matters
Pediatric ulcerative colitis is rising, and diet plays a role in managing it. Learning whether sulfite preservatives disrupt mitochondria and repair of the colon lining, especially in children with reduced Mocs1, could inform dietary advice for young UC patients and their families.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
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.
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
University of Alabama at Birmingham: 45 labs on PI Pages, $866M a year on research, 166 research doctorates a year.
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