Christina Leigh Stallings
Washington University in St Louis, MO·Microbiology & Immunology
Tuberculosis, caused by the bacterium Mycobacterium tuberculosis, kills more people than any other infectious disease, and drug-resistant strains are making existing treatments less reliable. Research in this lab asks two linked questions: which immune responses actually help the body control the bacterium (and which ones backfire and help it grow), and whether new chemical compounds can kill it through mechanisms that current drugs do not use.
- Fields
Microbiology & Immunology
Pharmacology
Medicine & Clinical Research
- Topics
tuberculosis
Mtb
alveolar macrophages
- Grants
- 4 known grants, through Mar 2030
What they work on
- 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.
- Test the relationship between SPTLC2, clearance of pulmonary surfactant from the air sacs, and control of M. tuberculosis, and identify which specific sphingolipid species sustain lung function during infection.
- Map type I interferon and DAMP (damage-associated molecular pattern) signaling in innate immune cells in the first hours after macrophage infection, testing whether a self-propagating loop between them drives granuloma formation.
- Dissect the molecular basis of the interferon-DAMP loop to find points where drugs could redirect early immune responses toward controlling the bacterium, and determine how HIV infection amplifies the loop.
- Determine how NETosis — neutrophil release of chromatin-based extracellular traps — is regulated during Mtb infection, focusing on the histone-modifying enzyme PAD4, type I interferon, and the suppressive role of ATG5.
- Test how neutrophil extracellular traps promote M. tuberculosis replication and loss of infection control, using genetic and chemical inhibition of NETosis in cultured cells and in mice.
- Optimize nitro- and chloro-1,2,4-triazole and pyrrolidine compounds for drug-like pharmacological properties and show preclinical proof of concept against drug-sensitive and drug-resistant M. tuberculosis.
- Determine the mechanism of action of the chloro-1,2,4-triazole and pyrrolidine series, which stay active in F420- and Ddn-mutant bacteria that resist nitro-group prodrugs like pretomanid, to reveal new Mtb biology.
More about the research
The immunology projects focus on the lung's first-responder cells — alveolar macrophages, which engulf the bacterium, and neutrophils, which flood in afterward — while the chemistry project pushes a new class of antibacterial molecules toward preclinical proof of concept.
Why it matters
Tuberculosis causes roughly 10 million new cases and 1.5 million deaths a year and is the leading cause of death among people living with HIV, while drug resistance erodes current regimens. Two of these projects could identify host-directed therapies — drugs that dial down harmful neutrophil DNA traps or interferon-driven inflammation rather than attacking the bacterium — and one aims to deliver new antibacterial compounds effective against drug-resistant strains. Findings on alveolar macrophages and surfactant may also matter for patients with pulmonary alveolar proteinosis, who are prone to lung infections.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Investigating the roles for sphingolipid biosynthesis during lung infection
NIH · Jul 2026 – Mar 2030
Development of 1,2,4-Triazolyl Compounds and their derivatives as a New Treatment for Tuberculosis
NIH · Aug 2024 – Jul 2029
Type I IFN-dependent and independent contributions to the outcomes of early innate immune cell interactions during HIV/TB co-infection
NIH · Jul 2024 – Jun 2029
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.
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.
Avishek Mitra
Oklahoma State University, OK·Microbiology & Immunology
Determine how Rv0125, a protein Mtb releases outside the cell, strips heme from host hemoproteins such as hemoglobin, and whether it is a shared core component of the bacterium's heme uptake routes.
The school
Washington University in St Louis: 97 labs on PI Pages, $1.2B a year on research, 365 research doctorates a year.
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