Sara Suliman
University of California-San Francisco, CA·Microbiology & Immunology
Tuberculosis (TB) kills more people than any other infection caused by a single pathogen, the bacterium Mycobacterium tuberculosis (Mtb). Yet most people exposed to Mtb never fall ill.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Public Health & Epidemiology
- Topics
tuberculosis
cytomegalovirus
co-infection
- Grants
- 2 known grants, through May 2028
What they work on
- Determine how pre-infection with mouse cytomegalovirus one month before Mycobacterium tuberculosis affects survival, lung pathology and immune cell composition in C57BL/6 mice, using fluorescent reporter strains of both pathogens.
- Test whether CMV pre-infection raises susceptibility to Mtb in both infected and bystander macrophages, by sequentially infecting mouse bone marrow-derived and human monocyte-derived macrophages and measuring bacterial load and cell death.
- Map how co-infection rewires the lung using confocal microscopy, spectral cytometry and CITE-seq, which profiles single-cell gene activity plus surface proteins, in macrophage-enriched and whole-lung cell preparations.
- Test whether fumarylacetoacetate hydrolase (FAH), an enzyme in tyrosine breakdown, is required to control Mtb, by gene-editing FAH out of primary human myeloid cells and transferring fah-deficient fetal liver cells into TB-susceptible mice.
- Define the metabolic consequences of FAH deletion in Mtb-infected monocyte-derived dendritic cells and macrophages using metabolic flux experiments and complementation with individual tyrosine metabolites.
- Measure tyrosine metabolites by high-resolution mass spectrometry in banked plasma from a Peruvian TB cohort and link metabolic gene polymorphisms to metabolite levels in a longitudinal African household-contact cohort.
More about the research
Why outcomes differ so much is the question behind both projects here. One follows a common virus that reshapes the immune system before Mtb ever arrives; the other follows how infected cells handle tyrosine, one of the building blocks of protein. Both look at the host rather than the bacterium, with the goal of finding steps that could be blocked to prevent disease.
Why it matters
Knowing which people exposed to Mtb will progress to tuberculosis, and why, is central to preventing a disease that remains a leading infectious killer. Showing that impaired tyrosine breakdown drives risk could allow existing drugs for inherited tyrosine-metabolism disorders to be repurposed as preventive, host-directed TB treatments. An animal model of CMV-driven TB susceptibility could point to ways to interrupt the virus's contribution to disease in populations where both infections are common.
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.
Christina Leigh Stallings
Washington University in St Louis, MO·Microbiology & Immunology
Define how SPTLC2, the rate-limiting enzyme subunit for building sphingolipids, supports maintenance and monocyte-derived repopulation of alveolar macrophages during M. tuberculosis infection, using mice lacking Sptlc2 in CD11c+ lung cells.
Mushtaq Ahmed
University of Chicago, IL·Microbiology & Immunology
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.
The school
University of California-San Francisco: 89 labs on PI Pages, $2.1B a year on research, 164 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.