A realistic co-exposure scenario induces significantly high inflammation in lungs in NLRX1 dependent manner

Jessica Amedro*, Nairrita Majumder, Sherry Xie, and Salik Hussain
School of Medicine, Department of Microbiology, Immunology and Cell Biology, Department of Physiology and Pharmacology, West Virginia University, Morgantown, WV 26506

Presentation No.: 72

Assigned Category (Presentation Format): Health Sciences (Poster Presentations)

Student’s Major: Immunology and Medical Microbiology

Air pollution is among the five leading causes of premature deaths and cardiopulmonary hospitalizations. Air pollution is a complex mixture of gases and particulate matter. Recent epidemiological studies indicate that these components synergistically interact to induce adverse cardiopulmonary outcomes. We hypothesized that a realistic inhalation co-exposure to constituents of air pollution (ozone and ultrafine particles of carbon black) can significantly alter the lung inflammation via NLRX1, a member of Nod-like receptor (NLR) family. We exposed Nlrx1+/+ and Nlrx1-/- mice to air(controls) or CB+O3(2.5mg/m3+1ppm) for 3 hours followed by sacrifice after 24 hours. We observed significant changes in lung inflammation, alveolar barrier damage, airway hyper responsiveness and lung function decline in Nlrx1-/- compared to Nlrx1+/+. Our studies demonstrated significant increase in inflammatory cells (neutrophils) in lavage, increased inflammatory gene (TNF-α, IL-6) expression and airway hyperresponsiveness in Nlrx1-/- mice post co-exposure with CB and ozone. In conclusion, we demonstrate that NLRX1 is involved in control of carbon black and ozone induced lung toxicity. Further studies are ongoing to evaluate signaling pathways implicated in these increased inflammatory responses.

Funding: NIH

Program/mechanism supporting research/creative efforts: the WVU IMMB Undergraduate Research Internship Program (Jennifer Franko)