Katherine Broderick
Pronouns: she/her
Research Mentor(s): Swati Bhattacharyya
Co-Presenter: Shah, Kris
Research Mentor School/College/Department: Internal Medicine, Rheumatology / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 2 – 11am – 11:50am
Room: League Ballroom
Authors: Katherine Broderick, Kris Shah, Swati Bhattacharyya, Syed Hasan
Presenter: 22
Abstract
Scleroderma is a life-threatening autoimmune disorder that causes chronic inflammation and an overproduction of collagen, leading to organ fibrosis with no therapy to date. Tissue damage from sustained injury can accumulate damage-associated molecular patterns (DAMPS) that activate immune signaling. An increased immune response can result from activation of the TREM-1 receptor in the body, resulting in increased proinflammatory cytokines. Before this study, it was not known whether blocking TREM-1 was beneficial in treating fibrosis. We observed the impacts of using GF9, a first-in-class inhibitory peptide, to block the TREM-1 receptor in bleomycin-induced mouse models of the skin and lung. The inhibition of TREM-1 proved to be an effective treatment, as it reduced activation of TREM-1 receptors and decreased production of proinflammatory cytokine mRNA in the skin of the mouse models. However, in this initial study, the inhibitor addition has not yet shown any significant impact on lung fibrosis. Though, the impact of increased inhibitors on other bodily functions should be further analyzed as mice lacking TREM-1 have a higher mortality rate. There should be additional research conducted using human fibroblasts along with mice models. An understanding of the inhibitors of fibrosis is important to a deeper understanding of this condition and the discovery of potential clinical treatments for those affected by the disease.
Biomedical Sciences
