Zharia Hunter
Research Mentor: Hannah Viola
Mentor Department: Biomedical Engineering, Engineering
Author(s): Not Available
Session: Session 3 (11:00 AM – 11:50 AM)
Presentation Type: Poster 39
Abstract
Idiopathic Pulmonary Fibrosis (IPF) is a progressive interstitial lung disease (ILD) characterized by scarring of airways which decreases lung function, leading to respiratory failure and death. There are limited therapies available, and those present mildly slow but do not reverse IPF. There is a need for a therapy that cooperates with innate immunity rather than repressing it, and this is where nanoparticle technology offers a solution. Nanoparticles (NPs) work as immunomodulators that control how innate immune cells respond to injury, turning these cells from profibrotic to proresolving. The aim of this study is to isolate macrophages, a common type of immune cell involved in fibrosis, in an in vitro setting to analyze interactions between these cells and two types of nanoparticles. This study is a follow up to in vivo studies where specific time point analysis was done, but the disease dynamics in between points were not a focus; thus, further examination of macrophage/NP interactions may lead to more insights on disease dynamics. This study was conducted by culturing several plates of macrophage cells derived from three different genomes: GFP-col, Wild type, and TLR-9. These cells were harvested from murine bone marrow and cultured to maturity. Once mature, cells were introduced to the nanoparticles therapy and the interactions were observed. The qualitative results were that none of the cell types expressed collagen when introduced to the nanoparticles, macrophages across all of the cell types were able to phagocytose nanoparticles, and liquid flushing was found to be an effective way to harvest marine marrow. The quantitative results indicated that all cell types were expressing a particular chemokine that related to unregulated pro-regenerative genes. These results show nanoparticles are not harmful to immune cells and reprogram genomic pathways to transform macrophage cells to be regenerative instead of fibrotic.
