Vishwanath Venketaraman
Western University of Health Sciences, CA·Microbiology & Immunology
Tuberculosis (TB) usually attacks the lungs, but its deadliest form, tuberculous meningitis (TBM), infects the membranes around the brain and spinal cord. Many patients die or suffer lasting nerve damage, and standard TB drugs, designed for lung disease, work poorly against it.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Pharmacology
- Topics
tuberculosis
tuberculous meningitis
Mtb
- Grants
- 1 known grant, through Mar 2027
What they work on
- Determine how glutathione (GSH) depletion in the central nervous system alters immune responses and increases susceptibility to tuberculous meningitis caused by Mycobacterium tuberculosis.
- Test whether restoring GSH, alone or alongside the TB drug rifampicin, improves control of Mtb infection, building on prior evidence that GSH boosts NK cell and T cell activity.
- Evaluate glutathione as an adjunctive immunotherapeutic agent that could prevent or improve treatment of TBM.
More about the research
People with TBM have very low levels of glutathione (GSH), a small sulfur-containing molecule that keeps cells' chemical balance. This raises the question of whether low GSH weakens the body's defenses and whether restoring it could help treatment.
Why it matters
Tuberculous meningitis kills many patients and leaves survivors with nerve damage, partly because current drugs are built for lung TB. Showing whether restoring glutathione improves immune control of TB in the nervous system could lay the groundwork for an add-on therapy given alongside drugs such as rifampicin. Over time this could help groups at high risk, including children and people with HIV.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sara Suliman
University of California-San Francisco, CA·Microbiology & Immunology
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.
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.
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.
The school
Western University of Health Sciences: 1 labs on PI Pages, $11M a year on research.
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