Interleukin-8 Impacts ECM Deposition of Airway Smooth Muscle Cells
Faculty Mentor Information
Dr. Sarah Wicher, College of Idaho
Presentation Date
7-16-2026
Abstract
Airway Smooth Muscle (ASM) cells line the trachea, bronchi, and bronchioles and contract to control airway diameter. ASM cells help regulate airflow and are involved in many respiratory conditions such as asthma. Interleukin-8 (IL-8) is a chemokine that promotes inflammation during an immune response and increases in the lungs with age. Our study aims to analyze how ASM cell deposition of extracellular matrix (ECM) proteins changes following treatment with IL-8. The ECM network includes components outside the cell that provide tissue structure and help regulate cell activities. In this study, we analyzed collagen I, collagen III, and fibronectin deposition by measuring the number of cells and how much of each protein was excreted. ASM cells were plated in a 96-well plate and treated with 0, 50, or 100 ng/mL of IL-8. Our results indicate an increase in fibronectin deposition at both 50 and 100 ng/mL of IL-8, while collagen I and collagen III deposition decreased at both 50 and 100 ng/mL of IL-8. Excessive fibronectin deposition could cause fibrosis that makes the tissue stiffer while decreased collagens I and III could reduce the cell’s structural integrity and ability to resist mechanical stress.
Interleukin-8 Impacts ECM Deposition of Airway Smooth Muscle Cells
Airway Smooth Muscle (ASM) cells line the trachea, bronchi, and bronchioles and contract to control airway diameter. ASM cells help regulate airflow and are involved in many respiratory conditions such as asthma. Interleukin-8 (IL-8) is a chemokine that promotes inflammation during an immune response and increases in the lungs with age. Our study aims to analyze how ASM cell deposition of extracellular matrix (ECM) proteins changes following treatment with IL-8. The ECM network includes components outside the cell that provide tissue structure and help regulate cell activities. In this study, we analyzed collagen I, collagen III, and fibronectin deposition by measuring the number of cells and how much of each protein was excreted. ASM cells were plated in a 96-well plate and treated with 0, 50, or 100 ng/mL of IL-8. Our results indicate an increase in fibronectin deposition at both 50 and 100 ng/mL of IL-8, while collagen I and collagen III deposition decreased at both 50 and 100 ng/mL of IL-8. Excessive fibronectin deposition could cause fibrosis that makes the tissue stiffer while decreased collagens I and III could reduce the cell’s structural integrity and ability to resist mechanical stress.