Davide Pisu
Tulane University of Louisiana, LA·Microbiology & Immunology
Tuberculosis begins when someone inhales Mycobacterium tuberculosis (Mtb), and the first cells the bacteria enter are alveolar macrophages, immune cells that patrol the air sacs of the lung. These cells were long viewed as a uniform population that offers the bacterium a comfortable place to grow.
- Fields
Microbiology & Immunology
Genetics
Medicine & Clinical Research
- Topics
tuberculosis
Mtb
alveolar macrophages
- Grants
- 1 known grant, through May 2027
What they work on
- Determine the host molecular mechanisms behind the blunted response of CD38-negative alveolar macrophages to Mycobacterium tuberculosis, using multi-omics profiling of chromatin organization and transcription factor activity after infection.
- Identify which epigenetic changes in lung alveolar macrophages are associated with long-term protection, by giving intranasal BCG vaccination before Mtb exposure and tracking the shift toward CD38-positive infected macrophages.
- Test with CRISPR-based gene perturbation in macrophages whether candidate host genes from existing datasets are required for the pro-inflammatory responses, including Nos2 expression, that restrict Mtb growth.
- Functionally validate additional host targets emerging from the chromatin and transcription factor analyses, using the same CRISPR perturbation approach in infected macrophages.
More about the research
Recent work from this team, using fluorescent Mtb strains that report on bacterial fitness together with single-cell RNA sequencing, which reads gene activity one cell at a time, shows a more complicated picture: the infected lung contains two main alveolar macrophage populations with very different outcomes for the bacteria. Understanding why one type fails to fight back could point toward ways of helping the immune system hold the infection in check.
Why it matters
Tuberculosis control depends on the immune system limiting bacterial growth in the lung from the earliest hours of infection. By defining why one group of alveolar macrophages fails to respond, and which epigenetic changes vaccination induces in them, this work could identify host targets for therapies or vaccine strategies that push lung macrophages toward containing Mtb rather than hosting it.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
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.
Nathan Schoettler
University of Chicago, IL·Microbiology & Immunology
Define the immune cell landscape in blood from Amish and Hutterite children using single-cell RNA sequencing, comparing cell type proportions and gene activity between the low-asthma and high-asthma farming populations.
The school
Tulane University of Louisiana: 17 labs on PI Pages, $276M a year on research, 187 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.