Michael Zuscik
University of Colorado Denver/Anschutz Medical Campus, CO·Microbiology & Immunology
Osteoarthritis (OA), the gradual breakdown of joint cartilage, is much more common in people with obesity. Extra weight on the joints is part of the reason, but inflammation linked to obesity also plays a role.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Physiology
- Topics
osteoarthritis
obesity
gut microbiome
- Grants
- 1 known grant, through Feb 2027
What they work on
- Test whether the obese, dysbiotic gut microbiome causes osteoarthritis by starting an inflammatory cascade that begins in the colon, spreads through the blood to the joint, and accelerates cartilage degeneration.
- Determine how the gut bacterium Bifidobacterium pseudolongum protects against obesity-related joint degeneration, testing whether expanding it reduces inflammation from colon to knee joint.
- Test whether the B. pseudolongum metabolome, the small molecules the bacterium produces, contains agents that suppress inflammation in the colon lining where obesity-related inflammation starts.
More about the research
This project asks whether the root cause sits in the gut. The idea is that an unhealthy shift in gut bacteria, called dysbiosis, sparks inflammation that spreads from the colon through the blood to the joints and speeds up OA. OA today can only be treated to ease symptoms, so a cause in the gut could open new ways to slow the disease.
Why it matters
Osteoarthritis affects people worldwide and is currently treated only to relieve symptoms. If gut dysbiosis drives the osteoarthritis of obesity, expanding the gut bacterium B. pseudolongum, for example with probiotics or prebiotic fiber, or delivering its anti-inflammatory metabolites could become new ways to slow joint degeneration in people with obesity.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sanja Novak
University of Arkansas for Medical Sciences, AR·Physiology
Evaluate how blood vessels in the synovium and subchondral bone change during OA development. Test whether early microvascular damage or later synovial angiogenesis drives cartilage damage, including after mechanical-stress knee injury.
Chia-Lung Wu
University of Rochester, NY·Biomedical Engineering
Determine how mechanical loading switches on WNT16 in chondrocytes through the force-sensing calcium channel TRPV4, by loading human stem cell-derived and hip chondrocytes in agarose gels and sequencing their genetic and epigenetic controls.
David Felson
Boston University, MA·Medicine & Clinical Research
Identify proteins in knee synovial fluid and plasma linked to knee pain and MRI-detected cartilage damage, using SOMAScan aptamer-based proteomics in about 500 paired samples from the MOST cohort.
The school
University of Colorado Denver/Anschutz Medical Campus: 41 labs on PI Pages, $766M a year on research, 205 research doctorates a year.
More about University of Colorado Denver/Anschutz Medical Campus
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