Nod-Like Receptor X-1 (NLRX1) is a Novel Mediator of Ozone-Induced Lung Inflammation

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 Category: Health Sciences (Poster Presentation #123)

Student’s Major: Immunology and Medical Microbiology

According to the World Health Organization, over 4 million deaths annually are attributed to outdoor environmental pollution. Ozone (O3) is one of the most reactive gaseous components of air pollution and is among six criteria pollutants identified/regulated by the US Environmental Protection Agency (EPA). Both epidemiological and experimental evidence confirm the ability of a short-term acute O3 exposure to aggravate pre-existing disorders such as asthma. We hypothesized that NLRX1, an antiinflammatory member of the Nod-like receptor (NLR) family, plays a significant role in O3-induced pulmonary inflammation. We exposed Nlrx1+/+ and Nlrx1-/- mice to filtered air (controls) or O3 (1 ppm) for 3 hours and euthanized the mice 24 hours post exposure. Bronchoalveolar lavage was performed to analyze cellularity and airway barrier permeability. Lung tissue were collected to measure cytokines (KC, IL-13, TSLP) gene expression (real time PCR) and protein expression (western blots/enzyme linked immunosorbent assay (ELISA)). Our studies demonstrated two to three fold increase in inflammatory cells (neutrophils) in lavage, increased inflammatory mediators gene and protein expression in Nlrx1-/- mice compared to Nlrx1+/+ mice post ozone exposure. In conclusion, we demonstrate that NLRX1 in involved in control of ozone induced inflammatory responses in the lungs. Further studies are ongoing to evaluate signaling pathways implicated in increased inflammatory response.

Funding: NIH

Program/mechanism supporting research/creative efforts: an external internship or other type of program