PIPages
Labs

David Durgan

Baylor College of Medicine, TX·Physiology

High blood pressure (hypertension) is the leading modifiable risk factor for heart disease, and an imbalance in gut bacteria, called gut dysbiosis, can help cause it. The proposed path runs from gut inflammation to inflammation in brain regions that control blood pressure, and then to hypertension.

Fields

Physiology

Microbiology & Immunology

Neuroscience

Topics

hypertension

high blood pressure

gut microbiota

Grants
1 known grant, through Nov 2028

What they work on

  1. Identify which gut bacteria produce extracellular vesicles that raise blood pressure, using a dilution scheme to simplify bacterial communities, and test the roles of vesicle flagellin and lipopolysaccharide.
  2. Determine how bacterial vesicles directly affect gut lining inflammation and barrier function using enteroids grown from normotensive WKY and hypertensive SHRSP rats.
  3. Define how bacterial vesicles alter microglia and neurons in the paraventricular nucleus using single-cell RNA sequencing, and deplete microglia to test whether neuroinflammation drives vesicle-induced hypertension.

More about the research

That requires the gut and brain to communicate, but how they do so in hypertension is poorly understood. This project tests whether tiny membrane bubbles shed by gut bacteria, called bacterial extracellular vesicles (EVs), carry these messages.

Why it matters

Hypertension affects many people and drives cardiovascular disease. If inflammatory vesicles from gut bacteria help raise blood pressure, they could become targets for new prevention and treatment approaches that change the gut microbiota, offering options beyond current blood pressure drugs.

Known grants

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

Bacterial extracellular vesicles in microbiota-brain communication and hypertension

NIH · Jan 2025 – Nov 2028

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Teresa A Milner

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Test whether altered GluA1 signaling in PVN neurons contributes to angiotensin II-induced hypertension in post-AOF mice. GluA1 is part of AMPA glutamate receptors, which relay fast excitatory signals between neurons.

Kafait U Malik

University of Tennessee Health Science Center, TN·Pharmacology

Determine how the brain's arachidonic acid/ALOX15 pathway in the paraventricular nucleus contributes to angiotensin II-induced hypertension in female and male mice, using adenovirus gene tools and radiotelemetry.

The school

Baylor College of Medicine: 38 labs on PI Pages, $881M a year on research, 115 research doctorates a year.

More about Baylor College of Medicine

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