Kenneth Remy
Case Western Reserve University, OH·Medicine & Clinical Research
Red blood cells carry hemoglobin, the iron-containing protein that moves oxygen, and its iron-binding core is called heme. When red cells break apart (hemolysis) or are given by transfusion, hemoglobin and heme can leak into the blood plasma.
- Fields
Medicine & Clinical Research
Microbiology & Immunology
Physiology
- Topics
heme
cell-free hemoglobin
hemolysis
- Grants
- 4 known grants, through Jul 2030
What they work on
- Measure how plasma proteins bind heme, the iron core of hemoglobin, during sepsis and after red blood cell transfusion compared with chronic hemolytic diseases and healthy conditions, using human patient samples.
- Test whether heme carried by different plasma binding molecules activates or suppresses innate and adaptive immune pathways, possibly via TLR4, an inflammation-triggering receptor, in human cells.
- Develop ex vivo strategies to scavenge circulating heme or block heme-immune pathways in human samples to reduce harmful immune changes in sepsis and sickle cell disease.
- Test whether people with HIV have more red blood cell-derived extracellular vesicles carrying cell-free hemoglobin than uninfected controls, and relate levels to cytokines, in 124 repository plasma samples.
- Determine whether these vesicles damage human aortic endothelial cells and activate platelets through reactive oxygen species and TLR4 signaling, using gene sequencing, flow cytometry and Seahorse metabolic assays.
- Validate a whole-blood ELISpot assay measuring IFN-γ and TNF-α release as a real-time readout of immune function in children with sepsis-induced multiple organ dysfunction across four children's hospitals.
- Combine repeated immune function tests with transcriptomic analysis to define immune endotypes in pediatric siMODS, link them to outcomes, and test candidate immune therapies on patient blood ex vivo.
More about the research
These projects ask whether that free heme and hemoglobin disturb the immune system and blood vessels, and how this could worsen outcomes in sepsis, sickle cell disease, critical illness and HIV. A second line of work measures how well the immune system of critically ill children is actually working, so that treatments can be matched to each patient.
Why it matters
Sepsis kills millions each year and lacks targeted therapies, and patients with sickle cell disease, thalassemia or transfusions face frequent infections. People with HIV keep an elevated heart disease risk despite treatment. This work could identify free heme and red-cell vesicles as treatable causes of immune and vascular damage, point to heme-scavenging strategies, and provide an ELISpot blood test to sort critically ill children into immune subgroups for precisely targeted clinical trials.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jamie Meegan
University of South Alabama, AL·Physiology·Early-career
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.
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.
Solomon Ofori-Acquah
Emory University, GA·Medicine & Clinical Research
Measure blood levels of HO-1, the heme-breaking enzyme, in sickle cell patients and transgenic mice, and test whether miR-494 and DNA methylation of the HMOX1 gene control it, by raising and lowering miR-494 in human blood immune cells.
The school
Case Western Reserve University: 34 labs on PI Pages, $643M a year on research, 213 research doctorates a year.
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