UC Riverside Undergraduate Research Journal

Organic dust, as found in agricultural farm work, is ranked among the highest occupational exposure hazards by the CDC. Agricultural dust containing endotoxins, pesticides, mold, and other chemicals, contributes to increased rates of respiratory diseases among these workers. Human bronchial epithelial cells (HBEC), which line upper airways, are frequently exposed to pathogens. Understanding the role of HBEC in inflammation following dust exposure (DE) is necessary to understand the mechanisms underlying inflammatory diseases. The complement system, a nonspecific and non-adaptable defense mechanism, is composed of circulating proteins that promote inflammation by attacking the cell membranes of pathogens and recruiting immune cells that secrete mediators of inflammation. We characterized complement protein expression in DE-treated HBEC using previously generated SWATH proteomics data and Western blotting. Western blotting identified that DE treatment in HBEC mediates the release and activation of C3, while data identified via SWATH-MS proteomics indicated significant upregulation of CD59—a regulator of complement activation. These data suggest that DE-HBEC may regulate complement activation and aim to elucidate the mechanisms by which HBEC promotes the complement system, and thus induce pulmonary inflammation in the presence of organic dust.