PIPages
Labs

Vincent Michael Bruno

University of Maryland, Baltimore, MD·Microbiology & Immunology

Mucormycosis is a deadly fungal infection caused by molds of the order Mucorales. People usually catch it by breathing in spores that are everywhere in nature.

Fields

Microbiology & Immunology

Medicine & Clinical Research

Pharmacology

Topics

mucormycosis

Mucorales

fungal infection

Grants
1 known grant, through Feb 2030

What they work on

  1. Determine the role of ANGPTL4, a protein produced downstream of the host hypoxia-response pathway, in Mucorales lung invasion, and test whether blocking it treats mucormycosis in mice.
  2. Use single-cell RNA sequencing of lung epithelial cells in infected mice to identify genes switched on by the hypoxia-response pathway during Mucorales infection.
  3. Characterize the newly identified pathway targets in cell culture and in mouse infection models to test how they contribute to fungal invasion.
  4. Evaluate the new host pathway targets as add-on therapies with current antifungal drugs in clinically relevant mouse models of pulmonary mucormycosis.

More about the research

Those most at risk include people with uncontrolled diabetes, transplant recipients, patients with leukemia and very low white blood cell counts, and people with severe trauma or burns. Only two antifungal drugs are approved: amphotericin B, which can damage the kidneys, and isavuconazole, which works no better. Even with disfiguring surgery to remove infected tissue, more than half of patients die. Instead of attacking the fungus, this project asks whether the body's own cellular machinery that the fungus exploits can be blocked.

Why it matters

Mucormycosis kills more than half of patients and up to 90–100% of those with prolonged neutropenia or widespread disease. It strikes people with diabetes, cancer, transplants and battlefield wounds. Targeting the host hypoxia-response pathway, including the ANGPTL4 protein, could yield new add-on therapies that work alongside existing antifungal drugs.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

Therapeutic targeting the host hypoxia-response pathway to treat Mucormycosis

NIH · Mar 2025 – Feb 2030

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Define how the Ryp1–4 transcription factors and the heat shock pathway, including the chaperone Hsp90, work together to drive temperature-triggered yeast growth and virulence in Histoplasma capsulatum.

Nancy Keller

University of Wisconsin-Madison, WI·Microbiology & Immunology

Determine the chemical products of isocyanide synthase (ICS) gene clusters that carry unusual enzymes or target proteins, using molecular and chemical analysis of fungi found by the lab's genome-mining pipeline.

The school

University of Maryland, Baltimore: 23 labs on PI Pages, $1.5B a year on research, 79 research doctorates a year.

More about University of Maryland, Baltimore

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