Brandt Pence
University of Memphis, TN·Microbiology & Immunology
Aging raises the risk of nearly every chronic disease and makes many infections more severe. A common thread is the innate immune system, the body's fast first line of defense.
- Fields
Microbiology & Immunology
Physiology
Medicine & Clinical Research
- Topics
aging
immunosenescence
monocytes
- Grants
- 1 known grant, last ended Aug 2026
What they work on
- Investigate how dysfunction of mitochondrial complex I, the first enzyme in the cell's energy chain, impairs inflammatory responses in monocytes from older adults, using human and mouse experiments.
- Test whether a mitochondrial transplant procedure can restore metabolic function in aged monocytes and reverse their weak inflammatory responses to infectious or inflammatory challenge.
- Carry out preclinical testing of mitochondrial transplantation as a simple, low-cost, cell-type-specific therapy for innate immune dysfunction in aging.
More about the research
With age it becomes both weaker at fighting infection, called immunosenescence, and chronically inflamed at a low level, called inflammaging. Monocytes are innate immune cells that circulate in the blood. In older people they release inflammatory signals at rest but respond poorly when actually challenged. Aged monocytes also have faulty mitochondria, the cell's energy-producing compartments, but no one has linked this to their immune problems.
Why it matters
Older adults face more severe infections and chronic diseases, partly because their innate immune cells malfunction. Defining how mitochondrial defects impair monocytes could reveal new therapeutic targets for conditions linked to inflammaging and immunosenescence. Mitochondrial transplantation could become a relatively inexpensive way to restore immune function in aging.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Daniela Frasca
University of Miami, FL·Microbiology & Immunology
Evaluate how aging changes the blood metabolite profile of people with HIV and how this relates to the function, features and gene activity of B cells, T cells and monocytes, using MACS/WIHS Combined Cohort Study (MWCCS) samples.
Arianne Theiss
University of Colorado Denver/Anschutz Medical Campus, CO·Microbiology & Immunology
Define how mitochondrial dysfunction expands CD74-positive inflammatory Paneth cells and disrupts gut balance, using mice lacking the mitochondrial protein PHB1 only in Paneth cells, which develop spontaneous ileitis.
Katrin I. Andreasson
Stanford University, CA·Neuroscience
Test whether reprogramming energy metabolism in aging microglia and blood macrophages, by blocking inflammatory PGE2 signaling, can prevent or reverse cognitive decline in aging and Alzheimer's model mice.
The school
University of Memphis: 3 labs on PI Pages, $109M a year on research, 180 research doctorates a year.
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