Mushtaq Ahmed
University of Chicago, IL·Microbiology & Immunology
Tuberculosis (TB), caused by the bacterium Mycobacterium tuberculosis (Mtb), infects about one-quarter of the world's population. Most infected people have latent TB: the bacteria persist without causing illness.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
- Topics
tuberculosis
Mtb
TB reactivation
- Grants
- 1 known grant, through Jun 2027
What they work on
- Determine whether bone morphogenetic protein (BMP) signaling, a lung development and repair pathway, is required to control Mycobacterium tuberculosis and prevent reactivation of latent TB.
- Characterize which cells activate the BMP pathway during latent TB, and the mechanisms they use, to explain how lung tissue repair and regeneration are linked to bacterial control.
- Test the hypothesis, based on RNA sequencing data across species, that latent TB controllers repair lung damage through BMP signaling without triggering strong inflammation.
More about the research
Still, 5–10% of latently infected people will go on to develop active disease. Little is known about what keeps the infection under control in most people, or what tips some toward disease. This project asks whether the lung's own repair systems help keep latent TB in check.
Why it matters
Hundreds of millions of people carry latent TB, and some will develop active, contagious disease. Understanding how BMP-driven lung repair helps keep the infection controlled could point to new therapies that stop latent TB from progressing to active disease. Such therapies could help people at risk of reactivation and support TB control worldwide.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sadiya Parveen-Nesson
Louisiana State University, LA·Microbiology & Immunology
Test whether blocking glutaminase (GLS1), the enzyme that breaks down glutamine, restores the TB-killing ability of Mtb-infected macrophages, using siRNA knockdown, chemical inhibition and macrophages from macrophage-specific GLS1 knockout mice.
John Chan
Rutgers University-New Brunswick, NJ·Microbiology & Immunology
Determine how B cells drive lung inflammation in chronic tuberculosis, testing whether they expand CD4+ helper T cells and interferon-gamma responses while suppressing the anti-inflammatory signal IL-10, using B cell-deficient, knockout and transgenic mouse strains.
Russell Kempker
Emory University, GA·Medicine & Clinical Research·Early-career
Identify the metabolic and lipid profiles of each region of human necrotic lung granulomas, using MALDI-2 mass spectrometry imaging and laser capture microdissection on surgically removed TB lung tissue.
The school
University of Chicago: 39 labs on PI Pages, $681M a year on research, 457 research doctorates a year.
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