Jamie Meegan
University of South Alabama, AL·Physiology·Early-career
In sepsis, the body's reaction to an infection spirals out of control and blood vessels throughout the body begin to leak. The thin layer of endothelial cells lining the smallest vessels normally acts as a barrier; when it fails, fluid floods into tissues, organs stop working and patients can die.
- Fields
Physiology
Medicine & Clinical Research
Pharmacology
- Topics
sepsis
acute respiratory distress syndrome
acute lung injury
- Grants
- 1 known grant, through Jul 2027
What they work on
- Test whether cell-free hemoglobin released from fragile red blood cells during sepsis disrupts the lung microvascular endothelial cell barrier by oxidizing low-density lipoprotein to oxidized LDL.
- Determine how oxidized LDL signaling through its endothelial receptor LOX-1 (lectin-like oxidized LDL receptor 1) causes hyperpermeability in lung microvascular endothelial cells during sepsis.
- Examine whether LOX-1 ectodomain shedding, the cleavage of the receptor's outer portion, contributes to endothelial barrier failure and lung injury.
- Relate circulating cell-free hemoglobin and oxidized LDL levels in patients with sepsis to markers of microvascular endothelial injury and to mortality.
More about the research
In the lungs this leak drives acute respiratory distress syndrome (ARDS), a condition with no specific prevention or treatment. Understanding what molecules break the barrier is the route to a targeted therapy.
Why it matters
Sepsis kills through organ failure driven by leaking blood vessels, and sepsis-related acute respiratory distress syndrome has no specific treatment. If oxidation of LDL by cell-free hemoglobin and signaling through the LOX-1 receptor prove to drive lung vascular leak, each step becomes a candidate drug target, and the circulating levels of hemoglobin and oxidized LDL could help identify patients at highest risk.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Patrick Belvitch
University of Illinois Chicago, IL·Medicine & Clinical Research
Determine how CARMIL1, a regulator of actin filament growth, shapes edge actin structures in lung endothelial cells, using biochemistry and advanced imaging after silencing CARMIL1 or overexpressing normal or variant forms.
James Ross
Case Western Reserve University, OH·Medicine & Clinical Research·Early-career
Define how free hemoglobin lowers nitric oxide availability and triggers endothelial injury in human endothelial cell models, and test whether haptoglobin, a hemoglobin-binding protein, reduces these effects.
Lee Quinton
University of Massachusetts Chan Medical School, MA·Microbiology & Immunology
Map when and where CD4+ resident memory T cells, immune cells that stay in previously infected lungs, become activated near airways and veins while neutrophils spread through the lung, using imaging and cytometry in mouse pneumonia.
The school
University of South Alabama: 5 labs on PI Pages, $70M a year on research, 53 research doctorates a year.
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