Maggie Lomasney
Pronouns: she/her
Research Mentor(s): Daniel Eitzman
Co-Presenter:
Research Mentor School/College/Department: Internal Medicine – Cardiology / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 6 – 4:40pm – 5:30 pm
Room: League Ballroom
Authors: Maggie Lomasney, Jessica Venugopal, Daniel Eitzman, Chiao Guo
Presenter: 1
Abstract
Sickle cell disease (SCD) is associated with chronic hemolytic anemia and secondary activation of inflammatory cascades that may contribute to comorbidities. IL1R receptor activation following binding to ligands IL-1ß or IL-1a may be particularly important in SCD complications, however, the causal role of each of these factors remains to be determined. To determine causal effects of IL-1R signaling in SCD, SCD mice were generated with genetic deficiency states of either IL-1R, IL-1ß, or IL-1a, and then phenotyped. Circulating blood cell numbers were assessed in mice at 6 weeks and at 9 weeks of age. Additionally at 9 weeks, percent circulating reticulocytes and percent sickle erythrocytes were assessed as well as the weight of the spleen, kidneys, and liver. Formalin fixed organs were embedded and tissue slides were stained with Perl’s blue for iron. At 9 weeks of age, anemia in mice with deficiency of the IL-1R was similar to control mice, measured by hemoglobin, red blood cell counts, and erythrocytes. Mice with deficiency of IL-1B showed less severe anemia with a lower spleen weight as a percentage of total body mass in males, increased red blood cells (rbc), and decreased reticulocytes, although these positive results were not seen in the female mice null for IL-1b protein. IL-1a null SCD mice had lower rbc hemoglobin and hematocrit than IL-1a replete mice. IL-1a null males had increased sickling and increased circulating reticulocytes. In conclusion, IL-1R signaling in SCD may lead to both beneficial and harmful consequences related to anemia and comorbidities, depending on specific-ligand interactions. Additional studies are warranted to confirm and further characterize mechanisms involved in IL1R signaling prior to pharmacologic intervention studies in humans.
Biomedical Sciences
